The causes of inflammatory bowel disease (IBD) are poorly understood, but now, scientists have pinpointed a runaway immune response that may underlie the condition in some patients.

IBD, which is characterized by chronic inflammation in all or part of the digestive tract, affects millions of people worldwide. Its principal forms are Crohn's disease, which can occur at any point of the gastrointestinal tract, and ulcerative colitis, which affects only the colon and rectum.

While IBD patients may experience similar inflammation, the underlying cause may be different. Understanding those differences could potentially unlock new, targeted angles for treatment, researchers concluded in the new study.

"Identifying these patients early could eventually allow clinicians to move more quickly toward therapies that address the specific mechanism of disease rather than relying on a trial-and-error sequence of medications," Dr. Brad Pasternak, medical director of the IBD Clinic at Phoenix Children's Hospital, who was not involved in the work, told Live Science in an email.

A potential subtype of IBD

The genetics of IBD are complex, with past studies linking the condition to 300 "hotspots" throughout the genome. The strongest known genetic risk factor for ulcerative colitis is a gene variant called HLA-DRB1*01:03, but how this variant contributes to IBD has been unclear.

The new study, published June 10 in The New England Journal of Medicine, helps connect the dots.

A major clue had emerged in previous research by the same team, which tested the blood of two children with IBD. The kids had autoantibodies — immune proteins that target the body itself rather than germs — that were neutralizing a key anti-inflammatory protein called interleukin-10 (IL-10).

IL-10 normally works by inhibiting the secretion of pro-inflammatory proteins, so patients whose bodies block IL-10 are effectively releasing a brake that should be holding off inflammation, Pasternak said.

The researchers suspected that these autoantibodies could be one factor causing IBD. In their latest study, they sought to find out whether more IBD patients had the same autoantibodies.

The study included data from over 4,900 people with IBD and over 1,000 without the condition. Using two separate lab tests, the researchers analyzed blood samples from both groups, finding the autoantibody in 173 of the IBD patients, or about 3.5%. The autoantibody was virtually absent from the blood of the comparison group.

Then, in lab experiments, the team exposed immune cells to blood from the IBD patients who carried the autoantibody. This lowered the amount of IL-10 while triggering a pro-inflammatory response.

Study co-author Dr. Holm Uhlig, a pediatric gastroenterologist at the University of Oxford, told Live Science that identifying what drives the formation of the autoantibodies will be "a question of intense interest." For now, though, their data suggests that patients carrying HLA-DRB1*01:03 are far more likely to have autoantibodies blocking IL-10 than those without the variant.

Historically, the variant has been associated with severe IBD that can require major surgery to treat. "Currently, autoimmune responses are not at all part of the therapeutic repertoire, and that's why we feel it's a relevant study," Uhlig said.

Uhlig also noted that the subgroup of 3.5% of patients they identified is a "significant number," given the large overall number of IBD patients worldwide.

In general, many IBD patients are currently treated with therapies that broadly suppress inflammatory pathways, Pasternak said, but not everyone responds to treatment. This study points to a potential way to someday tailor treatments to the mechanism driving specific patients' diseases, he said.

Aside from offering personalized treatments for IBD patients, Uhlig said their findings may improve diagnoses.

"Patients could undergo genetic testing already in the early stage of their disease diagnosis," he said, "and then it would determine their susceptibility to develop autoantibodies."

This article is for informational purposes only and is not meant to offer medical advice.

The patient: A 23-year-old woman in Florida

The symptoms: The woman went to the emergency room with an itchy rash on her back that had lasted two days. The rash first appeared as isolated, inflamed regions on her upper back, which initially led her to seek treatment at an urgent care center. Despite treatment with steroids and antihistamines, however, the rash spread to the woman's lower back in grouped patterns of irregular stripes, which resembled lash marks made by a whip.

What happened next: When doctors examined the woman, they found "multiple streaked lesions on her back," according to a report of the case. The lesions were not blistered or peeling, and no other part of her body was affected.

The woman didn't report any other symptoms that are typically associated with an allergic reaction, such as difficulty breathing, throat irritation or swelling, or gastrointestinal distress. Nor was she experiencing body aches, joint swelling or any neurological symptoms. Her blood pressure, heart rate and respiratory rate were in the normal ranges, although her temperature was slightly elevated, at 99.1 degrees Fahrenheit (37.3 degrees Celsius).

In accordance with standard emergency-room procedures for patients with rashes, the doctors considered and eliminated possible causes for the lesions. The woman said the marks were not self-inflicted or made by someone else. She was not taking any medications besides those prescribed by the urgent care. She had not recently introduced potential skin irritants, such as new cosmetics, fragrances or detergents. She had not been bitten by insects and did not have a history of autoimmune disease or symptoms associated with meningitis, a disease that can cause rashes in addition to symptoms like neck stiffness and fever.

When the doctors asked the woman about foods she had eaten recently, she mentioned that the day before her symptoms appeared, she had eaten shiitake mushrooms.

The diagnosis: Although the woman had eaten shiitakes before and never had an adverse reaction, these mushrooms are known to occasionally cause a condition called shiitake dermatitis, a rash with a distinctive pattern that resembles whip marks.

Japanese researcher Takehiko Nakamura first described the condition in 1977, calling the lesions "flagellate dermatitis" after the flagellants, "a medieval religious sect whose members would whip themselves as a demonstration of their faith," according to the report of the woman's case.

The allergic response is thought to result from a compound in the mushroom called lentinan; in some people, lentinan causes the secretion of interleukin-1 and other cytokines, proteins that regulate inflammation as part of an immune response and can cause rashes. Researchers previously associated the rash with eating raw or undercooked shiitakes.

However, how the mushrooms are grown also may play a part, with log-grown shiitakes being more likely to cause a reaction than those grown on a substrate, the doctors noted.

The treatment: Doctors told the patient to continue using the medication that she received at urgent care: a topical cream containing hydrocortisone, a steroid to reduce inflammation; clotrimazole, which relieves fungal skin infections; and oral doses of diphenhydramine (an antihistamine) and methylprednisolone (a corticosteroid).

The woman was breastfeeding at the time, and she was worried that the cause of the rash might affect her breastmilk. However, the doctors reassured her that she could safely continue breastfeeding.

The medications provided some relief from her symptoms, which disappeared after about three weeks, she later reported at a follow-up visit. She also mentioned that she continued to regularly consume shiitake mushrooms and the whiplike rash did not reappear. (The authors of the report did not investigate or explain why she was not affected by shiitakes before or after this isolated incident.)

What makes the case unique: Shiitake dermatitis is rare, with approximately 100 reported incidents described in the scientific literature, according to the case report. Most of the reported cases occurred in Asia, and "although there have now been several cases in Europe and the Americas, it is still a relatively extraordinary occurrence in Western countries and the United States," the doctors wrote.

This article is for informational purposes only and is not meant to offer medical advice.

Can you guess the diagnosis in these strange medical cases? Find out with our diagnostic dilemma quiz!

The patient: A 17-year-old girl in California

The symptoms: The teenager went to an emergency department after experiencing vomiting episodes for about a day. Over the prior three months, she'd also had periodic shortness of breath accompanied by tightness in her chest.

What happened next: A test revealed that the patient's blood sugar was very high. It was 25.2 mmol/L (453 milligrams per deciliter (mg/dL)), whereas a normal blood sugar range for someone without diabetes is between 3.9 and 5.5 mmol/L (70 to 90 mg/dL). A hemoglobin A1C test, which measures average blood sugar levels over the past few months, delivered a result of 12%, with anything higher than 6.4% signaling diabetes.

Doctors learned that the patient had also experienced unusual thirst, excessive urination, unexplained weight loss and fatigue. Based on these symptoms and the high blood sugar, the doctors determined the patient likely had type 1 diabetes and admitted her to the pediatric department for further tests.

They started her on a conservative dose of insulin, but despite that, she often experienced low blood sugar in the mornings. And despite low fluid intake, she still urinated a lot, which is a characteristic symptom of uncontrolled diabetes.

The patient's mother also told doctors that the teen generally tended to "tan easily," though she didn't happen to have a tan at the time of the hospitalization.

"Given her atypical course and persistent findings," the doctors began looking into additional diagnoses that might explain these symptoms, they wrote in a report of the case.

The diagnosis: They considered whether the symptoms pointed to Addison's disease, which affects the adrenal glands located above the kidneys. These glands normally produce hormones that help control the stress response, blood pressure and water-salt balance in the body, but in patients with Addison's, they don't make enough of the hormones. This is most often caused by an autoimmune response, in which the immune system attacks the adrenal glands and undermines their function.

Tests showed that the patient carried antibodies against the adrenal glands, suggesting that such an autoimmune response was unfolding. Additionally, she had high levels of adrenocorticotropic hormone (ACTH), a signal the brain sends out in an attempt to crank up the activity of the adrenal glands; and renin, which the kidneys make when the body's water-salt balance is off.

At the same time, the brain also releases more of a hormone that drives up pigmentation in the skin, which can cause it to "tan."

These findings confirmed diagnoses of both type 1 diabetes and Addison's disease. Together, these diseases point to another, relatively rare condition called autoimmune polyendocrine syndrome type 2 (APS-2). This syndrome affects various hormone-making glands and is estimated to affect about 1.5 to 2 in 100,000 people.

The treatment: The patient received both short-acting and long-acting insulin to manage her diabetes. For Addison's disease, she was given a number of steroids to help boost levels of two key hormones: cortisol and aldosterone. These hormones, which are normally made by the adrenal glands, work together to manage blood pressure, fluid balance and stress responses. "This dose [of steroids] has been managing her symptoms well thus far," her doctors wrote.

Within two months of her diagnosis, she had begun gaining weight, her blood sugar levels had improved, and her ACTH and renin levels had normalized.

"Symptomatically, she has improved," the doctors wrote; "however, given the diagnosis [of] two autoimmune disorders requiring lifelong treatment, she has benefited from the emotional support from a counselor to cope with her new diagnoses and psychosocial stressors at home."

What makes the case unique: APS-2 is a relatively rare diagnosis, characterized by Addison's disease appearing alongside either type 1 diabetes, an autoimmune thyroid disease, or both.

The exact cause of the syndrome is not fully understood, but it has been tied to a number of gene variants, as well as environmental risk factors. Its presentation varies from patient to patient because different organs can be affected in each case. Patients often face delays in diagnosis due to this variation in disease presentation, the case reported authors noted.

"This case is unique because both diseases were diagnosed at the same time of presentation," they noted. "There are few cases that reported the concurrent diagnosis of T1DM [type 1 diabetes mellitus] and Addison's disease at initial presentation."

The case highlights the importance of screening patients with type 1 diabetes for additional autoimmune diseases, the doctors concluded. "Unexplained persistent electrolyte abnormalities" could raise a flag to screen for Addison's, they said, and that screening may include looking for adrenal antibodies, as they did in this case.

"Early detection could help prevent adrenal crisis, reducing morbidity and mortality associated with Addison's disease," they wrote.

For more intriguing medical cases, check out our Diagnostic Dilemma archives.

This article is for informational purposes only and is not meant to offer medical advice.

Keratin proteins form our skin, hair and nails — but when mutated, they can mess with the immune system, driving diseases like psoriasis and eczema, new research suggests.

In the new study, published Wednesday (April 8) in the journal Science Translational Medicine, researchers identified a mutant keratin protein that can disrupt processes that normally help skin cells manage inflammation. That breakdown could help to explain how inflammatory skin diseases emerge.

The research zoomed in on keratin 16, a form of keratin known to be mutated in a rare disease called pachyonychia congenita (PC) and previously linked to various inflammatory skin conditions. Study first author Erez Cohen, a postdoctoral researcher who studies cellular stress at the University of Michigan, and senior author Pierre Coulombe, chair of cell and developmental biology at University of Michigan Medical School, say their work could point to new therapies.

"Knowing that Keratin 16 acts as an inflammatory brake gives us a direct target for new treatments and diagnostics," they told Live Science in a joint statement.

Keratin's role in skin inflammation

The researchers focused on PC because the genetic disorder is known to be caused by mutations in the KRT16 gene, which carries instructions for keratin 16.

In PC, those mutations disrupt the network of filaments that helps skin cells in high-friction areas of the body, like the soles of the feet, resist mechanical stress. As a result, activities like walking or running cause skin cells to break down and become inflamed, forming painful calluses and blisters.

In people without PC, skin boosts its production of keratin 16 when facing stressors, such as inflammation.

"Keratins are like the steel cables or steel beams of the cell," Wendy Bollag, a professor in the Augusta University's department of physiology who wasn't involved with the study, told Live Science. "That tensile strength you need for the skin, [without it] it's prone to breaks, tears. Microorganisms can slip in and that will then cause the immune system to react and trigger inflammation."

And in people with chronic inflammation of the skin, the tissue continually makes lots of keratin 16.

"Understanding why these specific keratin proteins spike during inflammation and directly cause disease when mutated has the potential to identify new ways to treat PC, psoriasis and related conditions," Cohen and Coulombe said.

So Cohen, Coulombe and colleagues aimed to uncover the mechanism between keratin 16 and PC. They looked at samples of thickened skin from patients with PC, as well as samples from lab mice with a similar condition. They also disabled the KRT16 gene in a second group of mice to see what would happen if the gene didn't work at all.

They found that when the keratin 16 gene was mutated or missing, skin inflammation skyrocketed. According to Cohen and Coulombe, these results suggested that "K16 normally acts as a 'brake' on the signals produced by skin cells to recruit the immune system."

These signals included type I interferons, a family of proteins that help control inflammation and orchestrate immune responses against viruses and cancer.

In both patients and mice with PC, type I interferon signaling was more active than in people and mice without the condition, the researchers found. The same increase was seen in the mice with no keratin 16, suggesting that when the protein is absent, interferons activate a robust immune response and more inflammation.

On the flip side, when keratin 16 was present, these interferons' activity was modulated and the inflammation lessened.

Historically, keratin 16 has been "best known as a structural protein," Cohen and Coulombe said. Learning about this other function "completely changes how we view the skin's defense system and the role keratins play within it," they said.

Bollag noted that the study seemed thorough and its results compelling.

"This article is even more impressive than I thought in terms of all of the different techniques and approaches that were used to show that keratin 16 regulates interferon signaling in the skin," she said. "If you use multiple different techniques and multiple different approaches and they all confirm the same thing, that's a really powerful way to show that what you're looking at is real."

The study authors are optimistic that their findings could have big implications for future treatments for skin diseases. In fact, in the study, they demonstrated that an inhibitor of type I interferons helped clear up skin lesions in a mouse model of PC.

"Understanding this newly found connection creates an opportunity to examine type I interferon signaling as a new therapeutic target in PC," they said.

This article is for informational purposes only and not meant to offer medical advice.

Scientists have cured type 1 diabetes in mice, without long-term immune suppression.

In type 1 diabetes, the immune system attacks insulin-producing cells, and replacing them with transplanted cells from donors has historically required people to take strong immunosuppressants for life, which severely limited the reach of such transplants.

But in a new study, researchers created a "chimeric," or blended immune system that contains elements of both the recipient's and the donor's immune systems. This enabled mice to tolerate a transplant of insulin-producing cells without long-term immune suppression.

Much more research is needed before this kind of treatment could be available to patients in a clinic, and keeping the blended immune system balanced is tricky. But if extensive follow-up testing in humans shows the transplantation process is safe and durable, it could offer an avenue for reversing the potentially deadly disease.

"This is potentially a way to cure diabetes," Dr. John DiPersio, an oncologist at Washington University in St. Louis who researches cellular therapy but was not involved in the study, told Live Science. "It does represent, in theory, a big step forward."

Inducing intolerance

In type 1 diabetes, the immune system mistakenly attacks insulin-producing cells, or islets, in the pancreas. Without insulin, blood sugar rises and people eventually die, so people with the disease must take insulin for life. Even with the best treatment available, people with type 1 diabetes still face high rates of complications such as heart disease, kidney disease and eye damage.

For decades, scientists have been trying to cure the disease by replacing destroyed islets with new ones, such as those harvested from cadavers. But to keep the body from attacking the transplanted cells, patients must take strong immune-suppressing drugs for life. As a result, islet transplants are typically performed only in clinical trials and in patients who need another organ replacement, such as a kidney or liver transplant.

Using bone-marrow stem cells and islet cells from the same donor could solve the immune rejection problem. The stem cells, which are transplanted into special niches in the bone, would regenerate the white blood cells of the immune system. The new, regenerated immune system wouldn't have the islet-attacking cells and would recognize the transplanted islets as "self," rather than foreign.

But that process required eliminating the host's own bone-marrow stem cells. "It's like musical chairs," study lead author Dr. Judith Shizuru, a professor of medicine at Stanford University, told Live Science. "If you don't get the recipient stem cells out of the niche, you can't get the donor cells in."

In the past, the process required chemotherapy and radiation to completely wipe out the host's immune system, which leaves people vulnerable to infection for weeks.

Shizuru's team wondered if there was a less-toxic regimen that could reeducate the host's immune system, rather than erasing it. "If you have a mixture of donor and recipient, the donor's immune system ‪—‬ the blood system ‪—‬ can influence the behavior of the [immune cells] of the recipient," Shizuru said.

They came up with a multistep process that uses multiple antibodies, low-dose radiation and a rheumatoid arthritis drug called baricitinib, and tested that protocol in more than a dozen mice. This immune system "conditioning" process made space in the recipient's bone marrow for some donor stem cells, without wiping out all of the recipient's stem cells. It also muted different parts of the immune system just long enough for the donor's stem cells and islets to take root.

This allowed the team to transplant bone-marrow stem cells and islets ‪from the same donor into the recipient mouse. As the donor stem cells matured, the cells educated the rest of the recipient's immune system to tolerate the foreign tissue. The mature, blended immune system also culled recipient cells that had been trained to specifically attack islets, thereby eliminating the cells that fuel autoimmunity. "The graft sticks and stays," Shizuru said. "It's there long term."

From start to finish, the process took around 12 days, the immune system was never completely wiped out, and the radiation dose was lower than is typically used in bone-marrow transplants. "We've made this [a] much more gentle regimen," Shizuru said.

The mice were still making insulin 20 weeks later, and blood tests and postmortem analysis showed their immune systems were functioning well and not rejecting the transplants, the study authors noted in the paper, which was published in the January issue of The Journal of Clinical Investigation.

Still, many hurdles remain before this could become a viable treatment in humans, said DiPersio, who was the author of an accompanying commentary piece in the same journal. First, some of the antibodies that worked in mice don't have approved analogues in humans, so this would need to be remedied. Second, the method requires getting both bone marrow and islets from the same donor, and the latter are already scarce.

But a thornier problem is that creating a mixed host-recipient immune system is a delicate balancing act, DiPersio said.

The researchers maintained this balance in mice, but they usually live just a year or two.

For this process to represent a cure, humans would need the different immune system elements to stay balanced for decades. "It's hard to do that over a long period of time," DiPersio said. If the balance shifted, the islets could gradually die or you could get a dangerous tissue rejection reaction, he said.

This article is for informational purposes and not designed to be used for medical advice.

Viruses found in the intestines — collectively called the gut virome — activate the immune system to help metabolize carbohydrates, thereby reducing blood sugar spikes, a new study in mice shows.

The findings, published March 11 in the journal Cell Host & Microbe, hint that the virome may play a role in metabolic disorders such as diabetes, the study authors said.

"Viruses are the most abundant entity in the body. There are more viruses than there are human cells, bacterial cells and any other cells," Jeremy Barr, a virologist at Monash University in Australia who was not involved in the study, told Live Science. "Yet their role is a huge black box."

The new findings lay the foundation for future virus-based therapies for diseases associated with changes to the community of microorganisms that exist inside the gut, Barr added.

Trillions of viruses thrive on and within different organs, including the gut, lungs, liver, kidneys and brain. Most of the viruses in the gut are bacteriophages, which infect bacteria and influence their growth, thus shaping the larger gut microbial ecosystem.

Past work showed that the composition of gut bacteriophages changes in metabolic disorders like obesity, nonalcoholic fatty liver disease and type 2 diabetes. This prompted Aikun Fu, a microbiologist at Zhejiang University in China, and his team to speculate that viruses that infect bacteria could influence how the body absorbs and digests nutrients ‪—‬ processes that are closely linked to metabolic health.

To test their hypothesis, the authors disrupted the gut viromes of mice, using an antiviral cocktail that primarily reduced bacteriophage levels, and fed the mice either a diet high in carbohydrates or one high in fats for 25 days. A disrupted gut virome had no noticeable effect on the digestion and absorption of nutrients in the animals that ate a high-fat diet. But mice that ate a high-carbohydrate diet had impaired sugar tolerance, even though the mice ramped up the expression of genes tied to carbohydrate digestion and absorption. These animals' guts broke down carbohydrates quickly, leading to a sharp rise in blood glucose levels — a hallmark of diabetes.

The antiviral cocktail did not affect the diversity or function of gut bacteria, indicating that the effects of the disrupted virome were independent of gut bacteria.

In a separate experiment, the team enriched the gut viral load in sterile mice that had no microbiome, either by transplanting viruses from the feces of another mouse or by directly injecting bacteriophages into the gut. In both cases, the mice showed improved glucose tolerance and reduced expression of carbohydrate digestion and absorption genes.

To understand how the bacteriophages brought about these metabolic changes, Fu and his team introduced fluorescent virus-like particles ‪—‬ viral proteins without the ability to replicate ‪—‬ into the mice's guts and observed that the viruses were taken up by T cells, a subset of immune cells. Follow-up analysis showed that the virome spurred the immune system to release proteins that prevent too much glucose from being ferried into the blood. Without the phages, this immune response is blunted and more sugar enters the blood rapidly.

The team repeated the experiments using human small-intestine organoids ‪—‬ tiny versions of the organ grown from stem cells in the lab ‪—‬ populated with human gut viruses. They observed a similar relationship between the virome, the immune system and carbohydrate metabolism.

"The fact that the virome can directly stimulate and activate carbohydrate metabolism, a fundamental energy uptake and conservation pathway, is completely novel," Barr said.

The study also suggests that researchers need to think about viruses when considering gut health, said Corinne Maurice, a microbiologist at McGill University who was not involved in the study. "They're showing that there are interactions between the virome and the immune system that we hadn't appreciated until now," Maurice told Live Science.

While the findings highlight the importance of viruses in carbohydrate metabolism, the researchers don't know how different types of viruses might affect the process.

Now, Fu wants to develop drugs or other strategies to alter the virome and, consequently, diseases like diabetes. However, experts emphasized that a lot of work still needs to be done to understand how the gut virome behaves in humans, across disease states, before any potential therapies are developed.

What if a single vaccine could offer protection against a range of disease-causing bacteria, common allergens and respiratory viruses? A new mouse study highlights an experimental vaccine that could potentially offer that elusive "universal" protection.

As it's been tested only in lab animals, the vaccine must still pass a number of trials in people before it can be proven safe and effective.

The new study, published Thursday (Feb. 19) in the journal Science, describes a nasal-spray vaccine that works differently than most vaccines.

Conventionally, vaccines train the immune system to recognize a specific antigen, such as a protein on a virus's surface. The immune system then trains cells to remember and attack that antigen if they encounter it. This results in a robust, but fairly narrow immune defense — one which can be thwarted if the target antigen mutates over time.

Some scientists are working on vaccines that target antigens that are "highly conserved" between viral strains, meaning the antigen doesn't change much over time and looks similar from virus to virus. Such shots could potentially target many flu viruses or many coronaviruses at once, for example. But the scientists behind the new nasal-spray vaccine took a different approach: Rather than targeting only the "adaptive" immune system, which remembers specific antigens, it also revs up the innate immune system, a generic, first-line defense.

"What's remarkable about the innate system is that it can protect against a broad range of different microbes," senior study author Bali Pulendran, a professor of microbiology and immunology at the Stanford University School of Medicine, said in a statement.

The idea of a vaccine activating both innate and adaptive immunity is not completely new. It's well known that the tuberculosis vaccine, called Bacillus Calmette-Guérin (BCG), triggers this dual protection. In fact, because of that effect, scientists tested whether BCG could offer broad protection against COVID-19 in the early days of the pandemic.

Pulendran and colleagues had previously studied the BCG vaccine in mice and found that the shot caused immune cells in the lungs to spew specific signals. These signals prompted innate immune cells in the lungs to stay active for several months, rather than calming down after just days.

The new nasal-spray vaccine — called GLA-3M-052-LS+OVA — works by mimicking those special signals. It also contains a harmless egg-protein antigen that helps summon the right immune cells to the lungs. The team found that mice given three doses of the vaccine over three weeks were protected against SARS-CoV-2 (the virus that causes COVID-19) and other coronaviruses, the bacteria Staphylococcus aureus and Acinetobacter baumannii, and an allergen from house dust mites for at least three months afterward.

When exposed to these germs and the allergen, vaccinated mice were protected by the primed innate immune response and also quickly mounted an adaptive immune response against the insults. By comparison, unvaccinated mice fared much worse — in response to viruses and bacteria, they showed higher lung inflammation, weight loss and risk of death, and in response to allergens, they had more pronounced allergic reactions and mucus buildup.

"This is a really exciting piece of research," Daniela Ferreira, a professor of respiratory infection and vaccinology at the University of Oxford who was not involved in the study, told BBC News. It could "change how we protect people from common coughs, colds and other respiratory infections" if the results are confirmed in human studies, she said.

Pulendran also emphasized that, so far, the tests of the vaccine have been in lab animals and more work is required to translate the research to humans.

"If it ultimately proves safe and effective in humans, the potential impact could be transformative: simplifying seasonal vaccination and improving readiness for emerging respiratory threats," Pulendran told Genetic Engineering and Biotechnology News. Pulendran thinks two doses of the vaccine would likely be protective in people, according to the Stanford statement.

This article is for informational purposes only and is not meant to offer medical advice.

Around 90% of people are infected with Epstein-Barr virus at some point in their lifetimes. For most of them, the virus causes a mild, transient illness or no symptoms at all. But for a subset of people, Epstein-Barr can eventually contribute to chronic illnesses, such as lupus and multiple sclerosis, or to the development of cancer.

Now, new research uncovers 22 human genes that might make an Epstein-Barr infection more likely to turn into a chronic condition.

Researchers can't yet definitively say whether these genes directly make Epstein-Barr more dangerous, or whether they are part of an underlying immune suppression that allows the virus to persist at higher levels in the body than usual. But the new study should provide a jumping-off point, said Jill Hollenbach, a professor of neurology at the University of California, San Francisco, who was not involved in the study.

"My lab is already looking into the results and thinking about what we can learn from this and what other avenues of research it suggests," Hollenbach told Live Science. Hollenbach wrote a commentary of the new study accompanying its Jan. 18 publication in the journal Nature.

Nearly two dozen genes

Epstein-Barr virus can cause mononucleosis, better known as mono, a temporary illness notable for producing extreme fatigue. But even once the symptoms of mono disappear, the virus lies latent in the body, mostly in the immune system's B cells, which remember and defend against specific germs.

For most people, this latent Epstein-Barr virus causes no problems. But in other people, the virus persists at a higher, more active level. In these cases, it can raise the risk of certain nasopharyngeal cancers and lymphomas, and may fuel autoimmune disorders such as multiple sclerosis. Chronic, active Epstein-Barr has also been linked to heart and lung disease.

To understand why only some people seem to experience these chronic effects, Ryan Dhindsa at the Baylor College of Medicine and colleagues turned to an underexplored source of information: human DNA biobanks. These biobanks collect full gene sequencing data and health records for hundreds of thousands of individuals. In sequencing the human genome, they also happen to scoop up the DNA of any viruses that happen to be in residence inside cells.

"Typically, when we're analyzing human genome sequence data we ignore the reads that don't map back to a human reference genome. We just kind of throw them away," Dhindsa told Live Science. "Here, we decided maybe we could go through those reads that we normally throw away and see if we could recover viral DNA."

By combing through tossed-aside Epstein-Barr sequences from 750,000 people in the UK Biobank and the U.S. National Institutes of Health's All of Us biobank, the researchers were able to identify individuals — about 11% of the total — who had very high levels of Epstein-Barr DNA. They found that these high levels of viral DNA were associated with health conditions previously linked to Epstein-Barr, including diseases of the spleen and Hodgkin lymphoma.

The presence of viral DNA was also associated with conditions thought to be linked to Epstein-Barr, although less definitively: rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), and lupus. Other associations in the data reinforce even less well-studied connections, including links between Epstein Barr and heart disease, kidney failure, stroke and depressive episodes.

In addition, the researchers found 22 genes tied to a higher likelihood that someone would be in the 11% of people with chronic Epstein-Barr. Many of these genes were in a region of the genome called the human leukocyte antigen (HLA) locus, which is known to code for the immune cells that present antigens — immune-response-triggering foreign molecules — to other immune cells.

"It seems like these variants changed the way an individual's immune response actually presents Epstein-Barr virus to the immune system," Dhindsa said, possibly making it harder for the body to suppress viral replication. That said, the data has only shown a link between these genes and persistent infection — more research is needed to prove cause-and-effect.

In people with high levels of Epstein-Barr, the researchers also saw variations in genes that regulate the immune system. One, the SLAMF7 gene, typically encodes for a cell-surface protein that helps the immune system's natural killer cells attack tumors. Another, called CTLA4, encodes for a receptor on T cells that helps keep the immune system from attacking the body.

"They found some really interesting results," Hollenbach said.

She and her team are now interested in looking deeper at the mechanisms that link the genetic variation to the immune response to Epstein-Barr. Meanwhile, Dhindsa and his colleagues are interested in using biobank data to search for other viruses that have long-term impacts on human health. Some examples are the cancer-causing viruses Merkel cell polyomavirus and human T-cell lymphotropic virus type 1.

The researchers are also eager to expand their methods to more diverse global datasets of human genes. While the All of Us dataset includes participants from a variety of backgrounds, the U.K. Biobank is predominantly made up of people of European ancestry.

"We need to be able to look at genetic differences across more representative samples in future work," he said.

New laboratory experiments used "noses-in-a-dish" to unpack why the common cold triggers mild illness in some people while sending others to the hospital.

In the depths of cold and flu season, rhinoviruses — the most common cause of the common cold — make many of us miserable, causing symptoms like a runny nose, sore throat and mild cough. But for a subset of people, rhinovirus infections are a much more serious condition.

In smokers and people with asthma, for instance, rhinoviruses can lead to life-threatening breathing difficulties that require medical treatment. Even the same rhinovirus variant can cause wildly different medical outcomes depending on whom they infect.

Now, a new study published Jan. 19 in the journal Cell Press Blue has demonstrated that this variation depends on the activation of distinct immune programs inside the infected nasal tissue. The team grew miniature models of the human nasal passages in dishes to study how cells react to infection.

They say their findings are a step toward developing effective antivirals against the common cold.

How to grow a nose in a dish

The cells that bear the brunt of common cold infections are the epithelial cells lining the nose. When these cells detect a viral infection, they signal to the innate immune system — the body's first, nonspecific line of defense against germs. Some of the first defenders that this system deploys are molecules called interferons.

Despite knowing that interferons play an important role in fighting viruses, researchers have found it difficult to understand exactly how they do so at the cellular level.

The new research, led by Dr. Ellen Foxman, an associate professor of laboratory medicine and immunobiology at Yale University, used a technique called single-cell RNA sequencing, which reveals what information is being sent from a cell's control center that houses its DNA. They performed the analysis at the resolution of individual nasal epithelial cells.

Foxman's team grew these cells in a dish environment that closely resembled the inside of the human nose. Then, they infected the cells with a rhinovirus.

This pair of techniques enabled Foxman's team to gain new insight into how rhinoviruses affect nasal cells, said Clare Lloyd, a respiratory immunologist at Imperial College London who wasn't involved in the study.

"I think it's a combination of having a multicellular organoid [the nose-in-a-dish], as well as having these much more sensitive and specific techniques to allow us to be able to look at how ciliated cells are affected and how mucus-producing cells are affected," Lloyd told Live Science. Ciliated cells — which have tiny, hairlike projections — and mucus-producing cells are both found in the lining of the nose.

Foxman's initial observation was that, even when separated from the rest of the body, the nose cells were quite adept at fighting rhinoviruses.

"During an optimal response, viruses infect only ~1% of the cells, and the infection starts resolving within a few days," Foxman said in a statement. But when the team exposed the cells to a drug that suppressed interferon signaling, the cells' previously stout defenses began to crumble.

In these latter conditions, more than 30% of the cells became infected and the immune response became more pronounced. Levels of pro-inflammatory molecules, including cytokines, shot up, and there was a significant increase in mucus-protein production.

In the interferons' absence, one protein appeared to be the chief conductor of this overactive response: nuclear factor kappa B (NF-κB). The off-the-rails response resembled the reaction that often leads to complications of severe rhinovirus infection in vulnerable patients.

Lloyd said if a person is knocked flat by a rhinovirus infection, it may indicate issues with their interferon production. "Some people have genetic defects in interferon production … which may affect the tone of the interferon response they can generate," she said.

Lab studies like this are essential steps toward treating common viral infections, but Lloyd cautioned that antivirals targeting the immune response would have to manage a careful balancing act.

"The immune system is very nuanced," Lloyd said. "If you just completely block NF-κB, then you're blocking all kinds of cytokines and chemokines, so you're blocking the whole inflammatory response." Although inflammation can be harmful when it rages out of control, you do need some to combat infections effectively.

Foxman's group tested some antivirals on their cell models, including an experimental drug called rupintrivir. This drug was particularly effective at suppressing an overactive immune response, at least in the lab models. Rupintrivir had previously failed to suppress rhinovirus infections in clinical trials with patients. But still, the study authors suggested the drug might have a second life as a treatment to subdue overactive immune responses to viruses in vulnerable groups, such as patients with COPD (chronic obstructive pulmonary disease).

Mehul Suthar, a professor at Emory Vaccine Center who was not involved with the study, said drugs targeting the virus itself would be more precise than drugs that target an orchestrator of the immune response. Rupintrivir, for instance, targets viral proteins.

Rhinoviruses have remained a persistent pest for humanity because they can quickly evolve in response to treatments, thereby gaining resistance against them. It's only through a precise understanding of why colds make us ill that we can find a solution.

"It's obviously very challenging," Suthar said. "Otherwise, we'd have drugs for every virus out there."

A new mRNA treatment rejuvenates key immune cells in the body, which could help them fight off infections and cancer, a mouse study suggests.

T cells help train other immune cells to fight off disease. But as the body ages, the activity of these T cells declines, and they become less responsive to threats. Additionally, the thymus gland — where T cells mature — begins to shrink with age. These impacts of aging may explain why vaccines and immune-boosting cancer therapies don't work as well in older adults as they do in younger adults, Nature News reported.

In the new study, published Dec. 17 in the journal Nature, scientists tried to counteract these age-driven changes using messenger RNA (mRNA).

Among other roles, mRNA relays instructions from DNA to cells' protein-building organelles, serving as a template from which new proteins are made. The team behind the new study studied T cells in aging mice, pinpointing three proteins that seemed to decline with age, contributing to the aging process. They then generated mRNA for those three proteins, encased them in tiny bubbles of fat, and injected them into middle-aged mice, which were around 16 months old.

These mRNA-filled bubbles traveled through the bloodstream to the liver, where they accumulated. Most T cells are in the bloodstream, and because the liver filters blood, T cells were likely cycled through the liver, where they were exposed to this waiting supply of mRNA.

Mice treated with the mRNA made more T cells than mice that were left untreated. The treated mice's T cells also responded better to vaccination and to cancer immunotherapy, the experiments suggested.

The benefits of the treatment, which was given to the mice twice a week, disappeared quickly when the scientists paused the injections. That's not necessarily surprising, given that mRNA molecules degrade very quickly in the body, whether they were originally made by cells or produced in a lab.

"The transient nature of mRNA delivery necessitates repeated administrations to sustain therapeutic effects," the study authors wrote in the paper. That said, "the long-term consequences of continuous exposure to these factors, especially in aged individuals should be analysed through extensive long-term safety studies."

In short, more research is needed to see if the same approach could work in humans. You can read more about the study in Nature News.

Stress, anxiety and sleepless nights do more than erode peace of mind — they can also weaken the body's defenses, making people more susceptible to infections, cancers and autoimmune disorders. Now, scientists have uncovered a potential mechanism that may link these psychological factors and immunity issues.

In a new study, published Dec. 10 in the journal Frontiers in Immunology, researchers zeroed in on a type of immune cell called natural killer (NK) cells that may play a key role.

The research was partly inspired by a 2022 national screening study conducted in Saudi Arabia that showed generalized anxiety order (GAD) was on the rise, and that the trend was most pronounced in women. People with GAD experience constant, uncontrollable worrying, and their concern is typically more intense than the situation calls for; this can cause an array of related symptoms, including sleep problems.

This finding led immunologist and lead study author Renad Alhamawi at Taibah University in Medina, Saudi Arabia, to explore how anxiety might affect immunity among women.

Alhamawi and her colleagues recruited 60 female students between ages 17 and 23 and asked them to fill out a questionnaire about their mental health. The responses showed that 75% reported symptoms consistent with GAD — such as feeling nervous, being so restless that it's hard to sit still, or becoming easily irritable— including 13% with severe symptoms. (Although the participants were screened for GAD symptoms, none were officially diagnosed as part of this study.)

About 53% of the cohort, or 32 students, reported not getting enough sleep.

Next, the researchers took blood samples from the participants and surveyed the levels of various immune cells, which revealed that those who experienced anxiety-like symptoms had 38% fewer NK cells than those without symptoms.

NK cells are one of the first types of immune cells to respond to an infection or to the presence of cancer in the body, and immunologists split them into two subsets. The first subset secretes enzymes that break down and "kill" diseased cells. The second subset works by secreting protein signals, called cytokines, that regulate other immune cells. A reduced abundance of these dual-action cells could potentially predispose individuals to disease.

The participants who reported anxiety symptoms had reduced levels of both subsets of NK cells, while people reporting insufficient sleep had 40% fewer of the immune-regulating subset of cells only.

Importantly, this study found only a correlation between these anxiety symptoms, sleep and reduced NK cell levels; the researchers have yet to explore a causal link, let alone investigate whether this drop in NK cells could lead to markedly higher rates of disease.

It is not yet clear what factors might be behind this change in NK cell abundance in the bloodstream. For example, it could be that the cells die off or that the body renews them at a slower rate.

Also, "focusing on circulating NK cells [in the blood] does not allow investigation of NK cells infiltrating the nervous system," Stefano Garofalo, an immunologist at the Sapienza University of Rome who was not involved with the work, told Live Science in an email. He speculated that the drop in NK cells could happen if they migrate from the bloodstream into nerve tissue in people who have anxiety or insomnia. His research focuses on how NK cells help regulate brain function and shape behavior in mice.

These findings are consistent with those from other research, such as a study on chronic tinnitus, wherein participants who reported higher stress levels had fewer cell-killing NK cells. Alhamawi said that the stress hormone cortisol may drive down NK cell populations because it is known to exert other immune-suppressing effects. For instance, cortisol can hinder antigen-specific T cells, a type of immune cell that recognizes features of specific threats, like viruses.

"Anxiety increases the level of cortisol, so we think it might affect the number of NK cells in an indirect way," Alhamawi said.

The current research has a few caveats. "The main limitation of the study is the very small participant group, consisting exclusively of women under 25 years of age and belonging to a single ethnic background," Garofalo said. Future studies could determine if the correlation is more generalizable, using a larger mixed-sex population of individuals from different backgrounds.

Alhamawi noted that she would like to perform a long-term study, in which researchers track how anxiety, sleeping patterns and NK cell levels change over time in the same cohort of participants. That could provide a clearer picture of the relationship between these psychological factors and immunity, as well as the incidence of disease.

"We can see if there is [an] effect by testing if they develop more infectious disease or chronic disease," she added.

This article is for informational purposes only and is not meant to offer medical advice.

Scientists think a very common childhood infection may be linked to bladder cancer — and now, they're figuring out the chain reaction that connects the two diseases.

It's known that people who get kidney transplants are three times more likely to develop bladder cancer than the general population. Researchers have hypothesized that because transplant patients are immunosuppressed, dormant viruses lurking in the body are given the opportunity to reactivate.

These sleeping pathogens include BK virus (BKV), also called human polyomavirus type I, a common cold virus that 95% of people pick up as children. After an infection, the virus then lies dormant in the kidney. This introduces a question: Can the BK virus cause cancer years after it infects someone?

In a study published Dec. 3 in the journal Science Advances, researchers showed that the virus can cause the type of DNA damage that is also seen in bladder cancer that occurs later in life. But instead of finding DNA mutations directly caused by the virus, the researchers found that the culprit was the body's own immune system.

"This is a nicely-done laboratory study to show a possible way that BKV could have a larger role in bladder cancer than previously thought," Dr. Patrick Moore, a tumor virology researcher at the University of Pittsburgh who was not involved in the study, told Live Science in an email.

Connecting the dots

There are several types of viral infections that can lead to cancer. Some viruses, such as HPV, hijack the host cells of the infected person and insert their viral genetic material into the human genome, which causes the host cell to become cancerous. However, in some cancers, like those originating in the bladder, no detectable virus is present —but nonetheless, there are genetic signs of a previous viral infection.

"The long-running narrative since the 1950s has been that smoking and industrial exposures are the big cause of bladder cancer," said senior study author Simon Baker, a cancer researcher at the University of York in the U.K. But the patterns of DNA mutation seen in bladder cancers are different from those resulting from chemical carcinogens.

Instead, the cancers bear mutational signatures known to be caused by a family of enzymes called APOBEC. Normally, these enzymes help form the body's first-line defense against viruses and other pathogens. "They have these signatures from APOBECs, and we know APOBECs are part of the antiviral host defense," Baker explained.

Baker and his team took healthy human bladder cells and infected them with the BK virus in lab dishes. They found that the cells not only exhibited mutations similar to those seen in bladder cancer but also boosted the activity of APOBEC3, an enzyme that damages viral genomes in response to infection.

When the scientists turned off APOBEC3 and then infected the cells with the BK virus, the DNA damage didn't occur. This finding suggests that the enzyme made by the host cell was causing the damage, not the virus itself.

Additionally, the researchers found increased APOBEC3 expression and cancer-like genetic mutations in nearby "bystander" cells that hadn't been infected with the virus. So, a cell doesn't have to contain the actual virus to accumulate genetic mutations caused by an infection elsewhere in the body.

"That was a surprise," Baker said. "But the reason it makes perfect sense is that … bladder cancers don't have viruses in them." This finding starts to unravel the connection between early-life viral infections and cancers diagnosed decades later.

A starting point

Although these initial data are impactful, Moore said he would like to see whether patients with bladder cancer are infected more often with the BK virus than people without the cancer.

"It is intriguing," he said, "but only a starting point and work needs to be done to show its actual importance to human cancer."

When a person contracts the BK virus in childhood, they generally experience common cold symptoms before recovering. The virus then stays inactive, or dormant, in the kidney, bladder and tubes between the two organs. For most people, it never becomes an issue, and it's not routinely tested for outside of hospital settings.

For those about to have a kidney transplant, however, the immunosuppressants that prevent the rejection of their new kidney can also result in the reactivation of the BK virus, possibly damaging the kidneys, ureter and bladder in the process.

Tim Tavender, a kidney transplant patient from Southampton, developed a BK virus infection following his procedure and eventually had bladder cancer.

"Seeing this research makes me hopeful," Tavender told The Independent. "If scientists like Dr. Baker can find new ways to control BK virus, it could spare other people from going through what I did — and that would be life changing."

This article is for informational purposes only and is not meant to offer medical advice.

A new study helps reveal why some vaccines, including those for COVID-19 and influenza, are less effective in older adults than they are in younger people — and it may fundamentally shift our understanding of aging.

Traditionally, scientists have attributed the reduced vaccine response seen in older adults to a decline in the immune system with age. Many have pointed to persistent, low-grade immune activation — a process dubbed "inflammaging" — as one driver of this decline.

But a new study that compared the immune systems of older and younger adults found no consistent increases in biological markers of inflammation with age. Instead, aging appears to reprogram T cells — important immune cells that help train a type of white blood cell, called B cells, to produce antibodies in response to viruses and vaccines.

The findings, published Oct. 29 in the journal Nature, suggest that inflammation may not be as fundamental to the aging process as scientists previously thought.

"We think inflammation is driven by something independent from just the age of a person," Claire Gustafson, an assistant investigator at the Allen Institute for Immunology and one of the lead authors of the study, said in a statement.

Alan Cohen, an associate professor of environmental health sciences at Columbia University who studies aging and inflammation, said the new findings support a more nuanced view of "inflammaging."

The idea that inflammation increases with age "may be true on average in industrialized populations," said Cohen, who was not involved in the work. "But it won't be true for everyone, and it won't be true in every population," he told Live Science.

Cohen cautioned that the participants in the new study were drawn entirely from Palo Alto, California, and Seattle — both highly industrialized areas. Having found significant differences in inflammation between adult populations from Italy, Singapore, Bolivia and Malaysia, he said such findings may not hold up across different environments.

"I certainly wouldn't take this as, 'Oh look, now they've shown definitively there's no change in inflammation with age,'" Cohen said. "I would take it more as, here's an example of a population that doesn't appear to be doing the same things that we have typically expected."

T cell changes are not driven by inflammation

In the interest of improving older adults' responses to vaccines, Gustafson and her colleagues looked at how T cells change with age.

First, they compared younger adults (ages 25 to 35) with an older group (ages 55 to 65, or people at what the researchers call the "cusp of aging.") For two years, the researchers followed 96 healthy volunteers in these age groups, collecting blood samples from each participant eight to 10 times and monitoring their immune systems before and after their annual flu vaccinations. Then, they expanded their research to include a second group of 234 adults ranging in age from 40 to over 90.

To examine the immune system across these groups, the team used single-cell RNA sequencing, which enabled them to look at a type of genetic material called RNA inside each immune cell. RNA reflects which proteins a cell is making at a given moment. The team also used high-dimensional plasma proteomics, which maps the proteins circulating in blood, and spectral flow cytometry,which identifies and counts immune cells by their molecular "fingerprints."

The researchers spotted distinct differences in memory T cells — immune cells that "remember" past infections and help the body respond faster the next time a pathogen shows up.

In older adults, increasing numbers of memory T cells shift into a state that changes how they respond to threats — by changing their interaction with B cells. When memory T cells are not working as they should, B cells become less effective at producing antibodies in response to infections or vaccines, the study found. Meanwhile, the memory T cells of young adults were adept at responding quickly and ramping up the expected antibody response.

These immune changes seem to happen independently of inflammation and of infections with latent viruses, which stay in the body after the initial infection and may go dormant, not causing any overt symptoms. Infections with these viruses, such as cytomegalovirus (CMV), are often blamed for weakening the immune system with age. However, the study found that people under 65 who had experienced a CMV infection at some point in their life did not have signs of faster immune aging or increased levels of inflammatory proteins.

Cohen remains cautious about the study authors' conclusions, noting that the most significant changes in the immune system tend to occur after age 65. "If you don't see a change in inflammation between 25 to 35 versus 55 to 65, is that really because inflammation isn't changing with age, or just because they didn't get old enough to see something?" he questioned.

The researchers said these findings could eventually help scientists design vaccines that compensate for age-related immune changes, thus better protecting older adults. They also think the results could be useful for designing treatments that restore immune function in old age.

This article is for informational purposes only and is not meant to offer medical advice.

The COVID-19 mRNA-based vaccines that saved 2.5 million lives globally during the pandemic could help spark the immune system to fight cancer. This is the surprising takeaway of a new study that we and our colleagues published in the journal Nature.

While developing mRNA vaccines for patients with brain tumors in 2016, our team, led by pediatric oncologist Elias Sayour, discovered that mRNA can train immune systems to kill tumors — even if the mRNA is not related to cancer.

Based on this finding, we hypothesized that mRNA vaccines designed to target the SARS-CoV-2 virus that causes COVID-19 might also have antitumor effects.

So we looked at clinical outcomes for more than 1,000 late-stage melanoma and lung cancer patients treated with a type of immunotherapy called immune checkpoint inhibitors. This treatment is a common approach doctors use to train the immune system to kill cancer. It does this by blocking a protein that tumor cells make to turn off immune cells, enabling the immune system to continue killing cancer.

Remarkably, patients who received either the Pfizer or Moderna mRNA-based COVID-19 vaccine within 100 days of starting immunotherapy were more than twice as likely to be alive after three years compared with those who didn't receive either vaccine. Surprisingly, patients with tumors that don't typically respond well to immunotherapy also saw very strong benefits, with nearly fivefold improvement in three-year overall survival. This link between improved survival and receiving a COVID-19 mRNA vaccine remained strong even after we controlled for factors like disease severity and co-occurring conditions.

To understand the underlying mechanism, we turned to animal models. We found that COVID-19 mRNA vaccines act like an alarm, triggering the body's immune system to recognize and kill tumor cells and overcome the cancer's ability to turn off immune cells. When combined, vaccines and immune checkpoint inhibitors coordinate to unleash the full power of the immune system to kill cancer cells.

Why it matters

Immunotherapy with immune checkpoint inhibitors has revolutionized cancer treatment over the past decade by producing cures in many patients who were previously considered incurable. However, these therapies are ineffective in patients with "cold" tumors that successfully evade immune detection.

Our findings suggest that mRNA vaccines may provide just the spark the immune system needs to turn these "cold" tumors "hot." If validated in our upcoming clinical trial, our hope is that this widely available, low-cost intervention could extend the benefits of immunotherapy to millions of patients who otherwise would not benefit from this therapy.

What other research is being done

Unlike vaccines for infectious diseases, which are used to prevent an infection, therapeutic cancer vaccines are used to help train the immune systems of cancer patients to better fight tumors.

We and many others are currently working hard to make personalized mRNA vaccines for patients with cancer. This involves taking a small sample of a patient's tumor and using machine learning algorithms to predict which proteins in the tumor would be the best targets for a vaccine. However, this approach can be costly and difficult to manufacture.

In contrast, COVID-19 mRNA vaccines do not need to be personalized, are already widely available at low or no cost around the globe, and could be administered at any time during a patient's treatment. Our findings that COVID-19 mRNA vaccines have substantial antitumor effects bring hope that they could help extend the anti-cancer benefits of mRNA vaccines to all.

What's next

In pursuit of this goal, we are preparing to test this treatment strategy in patients with a nationwide clinical trial in people with lung cancer. People receiving an immune checkpoint inhibitor will be randomized to either receive a COVID-19 mRNA vaccine during treatment or not.

This study will tell us whether COVID-19 mRNA vaccines should be included as part of the standard of care for patients receiving an immune checkpoint inhibitor. Ultimately, we hope that this approach will help many patients who are treated with immune therapy, and especially those who currently lack effective treatment options.

This work exemplifies how a tool born from a global pandemic may provide a new weapon against cancer and rapidly extend the benefits of existing treatments to millions of patients. By harnessing a familiar vaccine in a new way, we hope to extend the lifesaving benefits of immunotherapy to cancer patients who were previously left behind.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

Scientists have discovered huge, mysterious pieces of DNA in the oral microbiome — the population of bacteria and other microbes living in our mouths — and they say this giant DNA might influence the human immune system.

It's well known that we have plenty of bacteria in our mouths and that these microbes can have both positive and negative impacts on our oral and overall health.

Now, in a study published Aug. 11 in the journal Nature Communications, researchers report a previously undiscovered feature of the oral microbiome: giant pieces of bacterial DNA that separate from the microbes' main genome. Moreover, these pieces of DNA are associated with changes in the body's immune system and even the occurrence of certain types of cancer, the team found.

The study provides a "new puzzle piece that is a step in understanding the oral microbiome, human health, and human disease," Floyd Dewhirst, a professor at the ADA Forsyth Institute who was not involved in the research, told Live Science in an email.

Microbiome studies, which have flourished in the past decade, have shown that the microbiomes across the body play major roles in human health and disease. Researchers have identified the types and proportions of different microbial species that live in places like our mouths and guts, and then used that data to see how differences in those features are linked to our health.

Over the years, the genomes of these species have been studied extensively but conventional genetic analyses have not yet been able to explain all of the links between our microbiome and overall health status.

Researchers in the Yutaka Suzuki lab at the University of Tokyo wanted to explore these missing data and were inspired by the recent discovery of giant extrachromosomal elements (ECEs) in bacteria living in soil. ECEs are pieces of DNA that are separate from an organism's main genome. In humans, our mitochondrial DNA — stored in the powerhouses of our cells — is an ECE. In bacteria, a commonly known small ECE is called a plasmid.

Lead study author Yuya Kiguchi, who is now a researcher at Stanford University, and his colleagues in the Suzuki lab predicted that giant ECEs could be found in bacteria living in places other than soil.

"Maybe many of these giant extra chromosomal elements are found in the environment, the microbiome field, or pathogens," Kiguchi told Live Science. "But we don't know any examples of this kind of giant extra chromosomal element from the commensal [human] microbiome." Commensal microbes are those that live symbiotically in or on the human body.

Using saliva samples from hundreds of people, the researchers found, for the first time, that giant ECEs also exist in our oral microbiome. The research team named these giant pieces of DNA "inocles;" the name stands for "insertion sequence encoded; oral origin; circle genomic structure." They also found that approximately 74% of people in their study possessed these inocles in their oral microbiome.

So why is this the first time inocles have been discovered? Most genetic experiments in bacteria use short-read DNA sequencing methods. This involves cutting a cell's DNA into smaller pieces, reading their code, and then assembling the bits into a full genome using a computer. While this method of sequencing can easily detect small ECEs, like typical bacterial plasmids, inocles are too large and complex for short-read sequencing to spot.

Using long-read DNA sequencing — a costlier and more time consuming method in which much larger pieces of DNA are sequenced and stitched together — the scientists could identify these large chunks of extrachromosomal DNA in the bacteria of human saliva samples. By correlating those results with blood samples from the same people, they also found that differences in the levels of inocles is associated with differences in the immune system, including the immune response to certain bacterial and viral infections.

Sixty-eight people in the study had either a type of head and neck or colorectal cancer, and these individuals had lower levels of inocles in their oral microbiomes compared with the people without these cancers. That raises the possibility of using these newly discovered giant chunks of DNA as future biomarkers for cancer, the study authors suggested.

As a next step, the researchers aim to grow these inocles in the lab so they can further investigate their function and how they can spread between bacteria and people.

"Now that we know that inocles exist, we can try and figure out their functions and potential roles in health and disease," Dewhirst said.

When the first cells appeared on Earth approximately 3.8 billion years ago, viruses were already here to greet them. Ever since, viruses have been devising ways to infect cells, and cells have been responding by evolving ways to stop these infections. This evolutionary dance eventually led to the development of your immune system.

A key aspect of your immune system is to distinguish "self" from "nonself" so it can destroy and remove foreign materials from your body. While this immune reaction protects you from viruses, it also has implications for how well foreign materials such as medications work.

I am a researcher studying ways to make drugs work better, including how to get them to the site of disease within the body before being removed or destroyed. One way to do this is to encapsulate drugs in nanoparticles — materials small enough to be taken up by cells. While these materials still trigger an immune response to get them out of the body, scientists like me have found that this reaction could actually be used to improve the effectiveness of cancer treatment.

The immune system and drug delivery

In addition to detecting pathogens, your immune system also responds to tissue damage. You might observe this reaction as inflammation — such as redness and swelling — when drugs are injected into your body with a needle.

Typically this inflammatory response is minimal. But the potential for a sustained reaction increases when drugs are administered slowly over a prolonged period of time, such as during chemotherapy infusions that can take an hour or more. For this reason, some patients are given anti-inflammatory medications before infusion to reduce the potential for an adverse immune response during treatment.

The most recent breakthroughs in getting drugs into the body is using nanoparticles. These materials — which can be made from lipids, proteins, gold or other components — have the advantage of being very small: The diameter of a typical nanoparticle is about 10-thousandths of a millimeter. Their small size allows diseased cells to easily take them up. So when nanoparticles contain drugs, they can act as a drug delivery system.

Despite being so small, nanoparticles can hold a large number of drug molecules, allowing them to deliver a potent cargo of treatment directly into a cell. They can also deliver drugs made of DNA and RNA. The most well-known example of this technology is the COVID-19 vaccine, which uses nanoparticles made of modified fat molecules to deliver mRNA that teaches the immune system to protect itself against COVID-19 infection.

Your innate immune system also identifies nanoparticles as foreign invaders when they are injected into your body. As a result, some patients experience an initial inflammatory reaction when the body tries to attack the nanoparticle.

But what if this reaction could actually be used to improve treatment?

Exploiting the innate immune response

For the past 30 years, my laboratory at the University of Colorado has been studying how nanoparticles deliver drugs. More recently, we have focused on understanding how the innate immune system responds to an injection of nanoparticles. While this immune reaction is typically considered a drawback, we wanted to explore whether it could enhance therapy.

In a 2022 study on how nanoparticles affect the immune response in mice, we found that the innate immune response triggered by an initial dose of nanoparticles carrying a drug will also reduce the effects of a second dose if it is injected shortly afterward — typically within days. It does this by clearing the drug out from the body more quickly. This reaction is similar to how an initial viral infection would trigger a short-term protective response against a subsequent infection from another virus.

One critical aspect of this protective effect involves the production of a protein called interferon lambda. This molecule "interferes" with the infection process by restricting viruses from gaining access to different tissues in the body. Researchers have previously tested this protein as a potential antiviral drug to treat COVID-19.

Similarly, the interferon lambda made in response to the first dose of nanoparticles limits the ability of the second dose to deliver the drug to healthy tissues in the body. However, it did not affect the nanoparticle's ability to access tumors, possibly because tumors can impair the immune response.

In conventional cancer treatment, chemotherapy drugs are used to kill the tumor. Because these drugs are also toxic to healthy cells, patients often experience side effects such as hair loss, gastrointestinal problems and skin rashes. Using nanoparticles to deliver cancer treatment could help reduce these side effects, and combining them with interferon lambda could allow the nanoparticle-encapsulated drug to stay in the body long enough to have its full effects.

Our team is studying whether directly injecting interferon lambda before chemotherapy with nanoparticles could help limit the amount of drug that ends up in healthy tissues while increasing their concentration in tumors. In an initial test of this strategy in mice with colon cancer, all mice that received interferon lambda saw increased survival time and reduced weight loss. A better understanding of how this effect happens could help researchers eventually test this approach to cancer treatment in human patients.

Scientists have a long way to go in developing nanoparticles that are as efficient as viruses at getting into cells. But our hope is that exploiting an immune response that evolved approximately a billion years ago to prevent viral infections could help reduce the toxic side effects from treatment while improving its effectiveness.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

A trio of researchers has won the 2025 Nobel Prize in Physiology or Medicine for discovering how the immune system is prevented from attacking our own bodies.

Mary E. Brunkow of the Institute for Systems Biology in Seattle, Fred Ramsdell of Sonoma Biotherapeutics in San Francisco, and Shimon Sakaguchi of Osaka University in Japan were awarded the prize "for their discoveries concerning peripheral immune tolerance." The Nobel Assembly at Karolinska Institutet announced the winners at a ceremony in Stockholm, Sweden, on Monday (Oct. 6).

The three scientists' research, honored with the 116th medicine prize, provides insights into keeping the immune system under control to fight microbes and avoid autoimmune diseases.

"Their discoveries have been decisive for our understanding of how the immune system functions and why we do not all develop serious autoimmune diseases," Olle Kämpe, chair of the Nobel Committee, said in a statement.

Our immune system has to protect the body from a variety of harmful microbes, acting like a biological bodyguard. Some sneaky invaders, such as viruses, can mimic human cells, so part of the immune system's job is to determine who is on the guest list, while kicking out anything that shouldn't be there.

The new Nobel Prize winners revealed how our bodies use regulatory T cells to keep the immune system in check. Their work has launched a new field in peripheral tolerance research and led to the development of new medical treatments, including for cancer and autoimmune diseases.

Sakaguchi made the first key peripheral immune tolerance discovery in 1995, when many researchers thought that the immune system only developed tolerance through a process called central tolerance, during which harmful immune cells are dealt with in the thymus — a specialized organ in the chest that makes white blood cells.

However, Sakaguchi demonstrated that the immune system has additional complexities by discovering immune cells, called regulatory T cells, that suppress overactive immune responses to protect the body's cells from autoimmune diseases.

These specialist cells keep an eye on other immune cells to ensure the immune system tolerates the body's natural tissues. In other words, they prevent our biological bodyguard from getting overzealous.

Brunkow and Ramsdell's contribution came six years later with their discovery that some mice had a gene mutation, named Foxp3, that makes them especially vulnerable to autoimmune diseases. The pair also found that alterations to the human version of this gene were responsible for immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome, an autoimmune disease.

In 2003, Sakaguchi demonstrated that the Foxp3 gene is responsible for governing the development of regulatory T cells.

Stay tuned for more Nobel Prize announcements this week. The next announcement will be on Tuesday (Oct. 7), when we'll learn who is awarded the 2025 Nobel Prize for Physics.

A universal cancer vaccine in development could help rev up the immune system against tumors and supercharge the effects of existing cancer therapies, an animal study suggests.

Similar to vaccines for viral infections like the flu, many cancer vaccines are designed to help the immune system recognize specific proteins. However, while conventional vaccines aim to prevent disease, cancer vaccines are currently being developed to clear away cancers already growing in the body and to help prevent treated cancers from coming back.

Nonetheless, conventional vaccines and cancer vaccines often work similarly. The flu shot trains the immune system to look for unique proteins found on the surface of influenza viruses, while cancer vaccines typically teach immune cells to spot unique features of cancer cells.

But there's a challenge: These cancer proteins of interest can often be unique to individual patients, meaning each cancer vaccine may need to be specially formulated for each patient. Although it's possible to craft such personalized vaccines, they take time to make — and, in the interim, the patient's cancer mutates, potentially causing the vaccine to be less effective.

"It can be months from the time you get a patient's specimen to when they actually have a personalized therapy," said study senior author Dr. Elias Sayour, a pediatric oncologist at University of Florida Health. Sayour and colleagues wondered if they could design a cancer vaccine that would not require this personalization and instead ignite a general immune response to keep cancer at bay.

"The idea that something could be available immediately, albeit in a nonspecific way … could be revolutionary for how we bridge therapy and how we manage patients," Sayour told Live Science.

Related: New mRNA vaccine for deadly brain cancer triggers a strong immune response

An "off-the-shelf" cancer vaccine

The experimental vaccine, described in a report published July 18 in the journal Nature Biomedical Engineering, is built upon messenger RNA (mRNA), which also formed the basis of the first COVID-19 vaccines that continue to be updated now.

mRNA acts as blueprints that cells then base new proteins on. In the COVID-19 vaccines, the molecule contains instructions for a bit of the coronavirus; in the new cancer vaccine, it carries instructions for a substance that raises the body's first-line immune defenses, poking the "innate" immune system rather than the "adaptive.".

In particular, the vaccine aims to boost the body's production of type-I interferons — immune messengers that play important roles in controlling inflammation and spotting cancerous tumors in order to eliminate them. In a series of experiments in lab mice, the researchers demonstrated that this signaling is key to snuffing out tumors early in their development. The signals help rally the immune system to attack the tumors and hinder the cancer's growth, and if you block them, tumor growth goes haywire.

Additionally, these experiments showed that this early interferon activity is vital to a common form of cancer treatment, called immune checkpoint inhibitors. These treatments rip the breaks off of immune cells so they maintain a high level of activity and kill off cancer efficiently.

Cancer has ways of hijacking interferon signals and thus thwarting the anti-cancer immune response that follows — so the cancer vaccine acts as a kind of immune "reset," Sayour explained.

The researchers used the vaccine in combination with a checkpoint inhibitor in a mouse model of melanoma, a type of skin cancer. In mice with treatment-resistant tumors, the combo of treatments worked better than checkpoint inhibitors alone, the team found. They also tested the vaccine on its own in mouse models of other cancers, including glioma (a brain cancer) and pulmonary osteosarcoma (bone cancer that's spread to the lungs). It showed promising anti-cancer effects when applied by itself, as well.

For this early work, the team tested a few different mRNA formulations to stir up the interferon response and found that each did so effectively. More work is needed to understand if the mRNA molecules themselves or the proteins they're used to make are more important for triggering this generalized response, Sayour noted.

The current study focused on solid tumors, which tend to be more resistant to immunotherapy than blood cancers are, Sayour said. But "I personally think this can be used for all forms of cancer," he added. "I believe this is a universal paradigm that can be used to treat cancer." In particular, he could see it being applied as secondary prevention, to help stop treated cancers from coming back.

"This exciting and novel paper shows promising evidence that giving the immune system a short, targeted boost at just the right time can help previously unresponsive tumors respond to immunotherapy," said Diana Azzam, an associate professor and scientific director at the Center for Advancing Personalized Cancer Treatments at Florida International University.

"This approach could be especially helpful for 'cold' tumors — types of cancer that usually don't trigger a strong immune response, like pancreatic, ovarian, and some types of breast cancer," Azzam, who was not involved in the study, told Live Science in an email. These tumors hide from the immune system and can be difficult to target with immunotherapy, so it's possible that this type of vaccine could help expose these cancers to attack.

"While more research is needed to confirm how well this approach will work in people, the encouraging results in mice offer a strong foundation," Azzam said. In people, you'd want to ensure that the vaccine mounts a helpful immune response without sparking unwanted inflammation in the long run, for instance. "Future studies will address key questions around safety, consistency, and long-term effectiveness in real-world cancer patients," she concluded.

Meanwhile, Sayour and his colleagues have launched a human trial testing a two-hit approach: an off-the-shelf cancer vaccine followed by a personalized one. They're working with patients with two types of recurrent cancers: either pediatric high-grade glioma or osteosarcoma.

"This approach saves valuable time needed for personalized vaccinations and may induce rapid immunity that can be further seized upon by personalized therapy," Sayour said.

This article is for informational purposes only and is not meant to offer medical advice.

Mitochondria have primarily been known as the energy-producing components of cells. But scientists are increasingly discovering that these small organelles do much more than just power cells. They are also involved in immune functions such as controlling inflammation, regulating cell death and responding to infections.

Research from my colleagues and I revealed that mitochondria play another key role in your immune response: sensing bacterial activity and helping neutrophils, a type of white blood cell, trap and kill them.

For the past 16 years, my research has focused on understanding the decisions immune cells make during infection and how the breakdown of these decision-making processes cause disease. My lab's recent findings shed light on why people with autoimmune diseases such as lupus may struggle to fight infections, revealing a potential link between dysfunctional mitochondria and weakened immune defenses.

The immune system's secret weapons

Neutrophils are the most abundant type of immune cell and serve as the immune system's first responders. One of their key defense mechanisms is releasing neutrophil extracellular traps, or NETs — weblike structures composed of DNA and antimicrobial proteins. These sticky NETs trap and neutralize invading microbes, preventing their spread in the body.

Until recently, scientists believed that NET formation was primarily triggered by cellular stress and damage. However, our study found that mitochondria can detect a specific bacterial byproduct — lactate — and use that signal to initiate NET formation.

Lactate is commonly associated with muscle fatigue in people. But in the context of bacterial infections, it plays a different role. Many bacteria release lactate as part of their own energy production. My team found that once bacteria are engulfed by a compartment of the cell called the phagosome, neutrophils can sense the presence of this lactate.

Related: 8 babies spared from potentially deadly inherited diseases through new IVF 'mitochondrial donation' trial

Inside the phagosome, this lactate communicates to the neutrophil that bacteria are present and that the antibacterial processes are not sufficient to kill these pathogens. When the mitochondria in neutrophil cells detect this lactate, they start signaling for the cell to get rid of the NETs that have entrapped bacteria. Once the bacteria are released outside the cell, other immune cells can kill them.

When we blocked the mitochondria's ability to sense lactate, neutrophils failed to produce NETs effectively. This meant bacteria were more likely to escape capture and proliferate, showing how crucial this mechanism is to immune defense. This process highlights an intricate dialogue between the bacteria's metabolism and the host cell's energy machinery.

What makes this finding surprising is that the mitochondria within cells are able to detect bacteria trapped in phagosomes, even though the microbes are enclosed in a separate space. Somehow, mitochondrial sensors can pick up cues from within these compartments — an impressive feat of cellular coordination.

Targeting mitochondria to fight infections

Our study is part of a growing field called immunometabolism, which explores how metabolism and immune function are deeply intertwined. Rather than viewing cellular metabolism as strictly a means to generate energy, researchers are now recognizing it as a central driver of immune decisions.

Mitochondria sit at the heart of this interaction. Their ability to sense, respond to and even shape the metabolic environment of a cell gives them a critical role in determining how and when immune responses are deployed.

For example, our findings provide a key reason why patients with a chronic autoimmune disease called systemic lupus erythematosus often suffer from recurrent infections. Mitochondria in the neutrophils of lupus patients fail to sense bacterial lactate properly. As a result, NET production was significantly reduced. This mitochondrial dysfunction could explain why lupus patients are more vulnerable to bacterial infections — even though their immune systems are constantly activated due to the disease.

This observation points to mitochondria's central role in balancing immune responses. It connects two seemingly unrelated issues: immune overactivity, as seen in lupus, and immune weakness like increased susceptibility to infection. When mitochondria work correctly, they help neutrophils mount an effective, targeted attack on bacteria. But when mitochondria are impaired, this system breaks down.

Our discovery that mitochondria can sense bacterial lactate to trigger NET formation opens up new possibilities for treating infections. For instance, drugs that enhance mitochondrial sensing could boost NET production in people with weakened immune systems. On the flip side, for conditions where NETs contribute to tissue damage — such as in severe COVID-19 or autoimmune diseases — it might be beneficial to limit this response.

Additionally, our study raises the question of whether other immune cells use similar mechanisms to sense microbial metabolites, and whether other bacterial byproducts might serve as immune signals. Understanding these pathways in more detail could lead to new treatments that modulate immune responses more precisely, reducing collateral damage while preserving antimicrobial defenses.

Mitochondria are not just the powerhouses of the cell — they are the immune system's watchtowers, alert to even the faintest metabolic signals of bacterial invaders. As researchers' understanding of their roles expands, so too does our appreciation for the complexity — and adaptability — of our cellular defenses.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

There may be an evolutionary thread linking big brains, long lifespans and immune-system genes in mammals, a new study finds.

An organism’s lifespan depends partly on its genes, but scientists have yet to pinpoint all of the genes that turn the dial on longevity. Long-living mammals tend to have larger brains, leading scientists to suspect that the same genes that boost longevity may also build bigger brains.

Now, in a study published April 29 in the journal Scientific Reports, scientists compared the genomes of 46 mammal species — including Homo sapiens — revealing a bevy of immunity genes that could be linked to both characteristics.

The maximum lifespan of a species refers to how long its members would live if they escaped environmental threats, such as predators or infections, and died only of old age. These lifespans vary considerably across mammals, from less than one year for the common shrew (Sorex araneus) to up to two centuries for the bowhead whale (Balaena mysticetus). The oldest person lived to 122, but one study suggests humans can reach age 150.

Related: Extreme longevity: The secret to living longer may be hiding with nuns... and jellyfish

Some genes linked to lifespan have already been found — for instance, elephants' genetics help guard against cancer. Due to their sheer size, elephants have more cells than other mammals and thus have greater odds of developing cancerous mutations. However, researchers discovered that these behemoths carry 19 additional copies of the gene for the tumor-preventing p53 protein, which enables them to live longer lives cancer-free.

Other genes for longevity remain to be discovered, so Araxi Urrutia, a geneticist at the National University of Mexico, and her colleagues set out to search for more. They wanted to focus on "families" of related genes.

Sometimes, when a cell copies its DNA and divides to form a new cell, it can accidentally copy and paste a gene to a new spot in the genome — a phenomenon called gene duplication. Over time, additional mutations cause the genes to become slightly dissimilar and adopt distinct functions.

If gene duplications occur multiple times within a group of related genes, they can produce a large family. One example is the beta-globin family of genes, which code for the proteins that make up hemoglobin, the oxygen-transporting molecule in blood. Urrutia's team wanted to assess if any of these duplicated-gene families contributed to longevity.

They looked at more than 4,100 gene families across 46 mammal species, including baboons (Papio anubis), cats (Felis catus), and dogs (Canis lupus).. Some mammals have higher-quality genome sequences available than others.

"Sometimes genomes are not sequenced in the same way, so they could introduce some noise" in the data, said lead study author Benjamin Padilla-Morales, a geneticist at the University of Bath in the U.K. To reduce the odds that any members of a given gene family were missing from the analysis, his team focused only on species that had at least 80% of their genome sequenced.

They also focused their analysis on gene families that were detected in at least 80% of the mammal genomes they studied, so they were common to many animals. This made it possible to see if the size of the gene family in a species was proportional to that animal's maximum lifespan.

They found that gene families involved in DNA repair and inflammation were small in short-lived mammals, whereas gene duplication had expanded those families in longer-living species. It may be that carrying more copies of DNA-repair genes can help prevent dysfunctional mutations from building up over time and thus promoting aging or cancer.

Related: Human aging accelerates dramatically at age 44 and 60

Meanwhile, genes involved in immunity may promote longevity by eliminating cancers early or fighting infections efficiently, said Maria Chikina, a computational biologist at the University of Pittsburgh who was not involved with the work. Some of the expanded genes in long-living species code for proinflammatory proteins, such as interleukin-6, which indirectly kickstarts antibody production. Chikina said these genes may also be involved in maintaining healthy tissue, such as by disposing of dead cells.

The immunity genes could additionally have roles unrelated to defense. "Many immune genes have been shown to be important in development, particularly in brain development," Urrutia said. Past research has linked brain size and longevity, and most of the immunity genes tied to lifespan in the recent study were also linked to bigger brains, she added.

Regarding humans, previous work pinpointed gene variants in centenarians — people who live to at least 100 — that may partially account for their long lives, and the new study revealed that many of these genes belonged to expanded gene families. This suggests these genes might be worth exploring further to understand how genes control human lifespan.

The study shows that the evolution of longer lifespans in mammals took place alongside the duplication of immunity genes. However, it wasn't possible to determine if these gene duplications caused the longer lifespans, Chikina noted. She suggested that, in the future, they could show that the association between these genes and lifespan is robust by repeating the experiment in nonmammals, like birds, to see if the connection holds true across more branches of the tree of life.

Chikina also proposed a way to test a causal link, to see if the genes actually drive up lifespan directly. "If you see there's some sort of interesting new gene popping up in long-lived species, you could put it in a mouse and see what happens," she said.

If further research can decipher if and how these genes affect longevity, scientists may one day be able to harness that information to develop anti-aging therapeutics or to predict the maximum lifespan of an individual based on their genetic makeup.

Disease name: Nocardiosis

Affected populations: Nocardiosis is a rare but potentially deadly infectious disease caused by bacteria in the genus Nocardia. Nocardiosis is an opportunistic infection, meaning it doesn't typically affect healthy people but may seize the chance to infect people with weakened immune systems, such as people with cancer or HIV/AIDS, as well as organ transplant recipients who are taking immunosuppressive drugs.

However, around 20% to 30% of patients with nocardiosis have no known pre-existing conditions, so the infection doesn't exclusively affect people with immune deficits. People over the age of 40, especially men, are also more likely to develop the disease than other demographics.

Between 500 and 1,000 new cases of nocardiosis are reported in the United States every year.

Related: Scientists have found a secret 'switch' that lets bacteria resist antibiotics — and it's been evading lab tests for decades

Causes: Nocardia bacteria are found in soil, standing water and decaying plant material. Around 100 Nocardia species have been identified so far, of which 12 are known to infect humans.

People may become infected with Nocardia bacteria when they inhale dust containing the microbes or they have a cut or scrape that comes in contact with contaminated soil or water.

Nocardiosis is not known to spread from one person to another; people pick it up directly from the environment.

Symptoms: The symptoms of nocardiosis vary depending on which part of the body is infected by Nocardia bacteria.

Most cases of nocardiosis start out as lung infections, in which pus-filled cavities, or abscesses containing the bacteria, form in the lungs. This can cause symptoms such as chest pain, a cough (including coughing up blood), sweats, chills and general weakness.

Nocardia bacteria can then travel in the bloodstream and form abscesses in other regions of the body, including the brain, kidneys and intestines. Infections of the brain can cause headache, weakness, confusion and seizures.

Approximately one-third of all patients infected with nocardiosis develop skin ulcers or sores, instead of an internal infection. These skin lesions typically form across the hands, chest wall or buttocks. They may look like open wounds or bumps under the skin.

Without treatment, nocardiosis can rapidly lead to death, often by causing organ failure or sepsis, a dangerous body-wide immune reaction. Between 16% and 40% of patients with nocardiosis die as a result of their infection. If the disease spreads to the brain, death rates jump to more than 80%.

Treatments: Nocardiosis can be treated with common antibiotics, although these bacteria are normally resistant to penicillin. The antibiotic treatment usually takes between six and 12 months to complete, and some patients may need to take antibiotics for even longer to prevent the disease from coming back.

Surgery may sometimes also be required to remove specific abscesses from the body, especially if a patient is not responding to antibiotic treatment.

This article is for informational purposes only and is not meant to offer medical advice.

A large proportion of East Asian people carry unique versions of the lactase gene that enables humans to digest the sugars in milk, new research hints.

These genetic variants were likely inherited from humans' extinct cousins, the Neanderthals, tens of thousands of years ago, according to a study published Mar. 10 in the journal PNAS. And it may be that the variants offered an evolutionary advantage by helping early hunter-gatherers thwart infections, new data suggest.

In some people of European or African descent, the lactase gene helps carriers digest a sugar called lactose in milk after they're weaned off of breast milk; this phenomenon is known as "lactase persistence." Many people who carry alternative versions of the gene can't continue breaking down lactose after infancy, so they become lactose intolerant.

The versions of the lactase gene behind lactase persistence are believed to have emerged in populations in Europe and Africa between 5,000 and 10,000 years ago, around the same time humans on these continents began rearing animals and consuming their milk.

Related: Papua New Guineans, genetically isolated for 50,000 years, carry Denisovan genes that help their immune system, study suggests

This has led scientists to theorize that the lactose-tolerance variants were selected for within these populations, meaning they became more common over the course of evolution because they offered an advantage. In this case, they may have increased survival rates by allowing adults to absorb nutrients from milk.

However, until now, little was known about the genetic mechanisms behind lactase persistence and lactose intolerance in East Asians. About 65% of adults worldwide are thought to be lactose intolerant, but this figure rises to between 70% and 100% in East Asian populations.

In the new study, scientists compared thousands of genomes sampled from modern humans, including those with East Asian, European or African ancestry. The data came from individuals in a range of countries, such as China, Japan, Spain, Italy and Nigeria.

The analysis revealed that around 25% of the people with East Asian ancestry carried versions of the lactase gene that are not found within the European or African populations. That's around the same proportion of people who have lactase persistence in East Asian populations. These genetic variants trigger an increase in the activity of the lactase gene in the body, the researchers found.

At first glance, this suggests that these genetic variants may have also been selected for during evolution for dietary reasons, the researchers said. However, further analyses in the same study revealed that this may not have been the case.

Indeed, the researchers went on to compare samples of East Asian genomes with the genome of a Neanderthal who lived in the Altai Mountains in Siberia around 120,000 years ago. This led them to discover that the East Asian variants of the lactase gene were likely inherited by hunter-gatherers from Neanderthals as a result of interbreeding events between the two groups.

Neanderthals and Homo sapiens are known to have interbred on multiple occasions over the millennia. This happened after both species came into contact with one another following the migration of the latter group out of Africa into Eurasia, possibly up to 250,000 years ago.

The new results suggest that the lactose-intolerance variants started being selected for between 25,000 and 28,000 years ago — more than 10,000 years before dairy culture emerged in the Altai Mountain region.

In other words, the variants emerged before people in the region started regularly consuming milk. This suggests that the selective pressure on these variants was not related to improving people's ability to digest lactose.

To figure out what other advantages these variants might offer, the team scoured a database chronicling gene activity in different cells. They discovered that the lactase gene variants seen in East Asian people altered the activity of three genes in immune cells, causing them to expand in number.

Based on this result, the study authors think it's possible that these variants were selected for because they somehow enhanced the ability of East Asian hunter-gatherers to combat infections.

"Neanderthals — having inhabited Eurasia for approximately 400,000 years — likely carried alleles [genetic variants] adapted to local pathogens and environmental challenges," study co-author Shuhua Xu, a professor of human population genetics at Fudan University in China, told Live Science in an email.

Taken together, the findings imply that variants of the lactase gene may have been selected for different reasons across the world, the researchers concluded. These findings may prompt scientists to question why selection of the lactase gene occurred in European and African populations, they added; perhaps the answer isn't solely about drinking milk.

Vaccines for infectious diseases have changed the trajectory of humankind. In the 20th century alone, smallpox killed more than 300 million people worldwide, and polio killed or paralyzed half a million people each year. Today, thanks to vaccines, smallpox has been eradicated worldwide, meaning it's essentially extinct; and polio has been eliminated in many countries, so the disease is no longer endemic to those places.

With the success of vaccines for infectious diseases in mind, scientists have wondered if it might be possible to similarly harness the power of the immune system against other conditions. Now, researchers are working to develop vaccines for cancer.

But what, exactly, are cancer vaccines, and how do they work?

Related: The 10 deadliest cancers, and why there's no cure

How do regular vaccines work?

Vaccines, broadly, are substances that train the immune system to defend the body against a dangerous invader. They help the immune system recognize a pathogen by exposing the body to key features of that germ, such as proteins from a virus's surface. These features are called antigens, and when they're introduced through a vaccine, the immune system learns to recognize them as a threat.

Once the immune system becomes familiar with antigens from a virus or bacterium, it will then be able to quickly mount an attack against that pathogen if it ever comes into contact with the bona fide germ. That's how vaccines stop people from contracting infectious diseases, such as smallpox or measles. If a vaccine doesn't completely block an infection from happening, it can still make the resulting illness much less dangerous — think of the annual flu shot.

"They [vaccines] harness the inbuilt ability of our immune systems to recognize something that is foreign to our bodies," Dr. Vinod Balachandran, director of the Olayan Center for Cancer Vaccines at Memorial Sloan Kettering Cancer Center, told Live Science.

Some common vaccines against infectious diseases already help prevent cancer. The human papillomavirus (HPV) vaccine, for example, protects against the strains of HPV that are most likely to cause cervical cancer, and the hepatitis B vaccine protects against liver cancer caused by chronic hepatitis B infections. But these vaccines don't actually target the cancer itself; they instead take aim at viruses that increase the risk of cancer.

How do cancer vaccines work?

In contrast, when scientists talk about a "cancer vaccine," they're referring to a vaccine that targets cancer directly, rather than using the indirect methods mentioned above, Balachandran said.

Harnessing the immune system to fight cancer with a vaccine is tricky, though, because vaccines rely on the immune system's recognition of a pathogen as a foreign invader. But cancer grows from our own cells — and that means the genetic and molecular compositions of a cancer cell are relatively similar to those of a healthy one.

However, certain molecules are found only in cancer cells, and researchers are attempting to use those molecules to train the immune system to fight cancer. They call these molecules neoantigens, and they're introduced to healthy cells through processes such as genetic mutation.

"If you can identify the neoantigens in a cancer that the immune system can recognize, you can teach the immune system to recognize a cancer as foreign," Balachandran explained.

There are some neoantigens that everyone with a certain type of cancer may have, but neoantigens can also be specific to an individual. Researchers are still investigating the most effective neoantigens to target for different types of cancer. Unlike vaccines for infectious diseases, Balachandran said, cancer vaccines will likely need to be designed for individual patients, or made in small batches, to ensure they're targeting these different neoantigens efficiently.

In his own lab, Balachandran is conducting small trials with human patients to develop a vaccine for a deadly form of pancreatic cancer. After surgically removing patients' tumors, Balachandran gave the participants a regimen of immune-boosting and chemotherapy drugs alongside a personalized vaccine that targets specific neoantigens seen in their tumors. The vaccines contain mRNA, a genetic molecule that, in this case, carries blueprints for the neoantigens. Once inside the patient, the vaccine enables cells to build those neoantigens and show them to the immune system.

Related: New mRNA vaccine for deadly brain cancer triggers a strong immune response

Half of the vaccinated patients in the 16-person trial showed a boost in cancer-fighting immune molecules, and their cancers didn't return for the duration of the 18-month study. These results suggest that, at least in some patients, personalized cancer vaccines could decrease the likelihood that deadly cancers will return.

Do cancer vaccines treat cancer, or do they prevent it?

Balachandran explained that currently, many cancer vaccines are targeted at what physicians call "secondary prevention." This means that they're designed to stop cancer from returning in a person that's currently in remission, rather than preventing cancer from emerging in the first place.

That said, there are also therapeutic cancer vaccines that can treat existing cancers. These work like immunotherapies for cancer, by revving up the immune system to fight tumors.

As of 2025, one therapeutic cancer vaccine has been approved by the U.S. Food and Drug Administration. This vaccine, called sipuleucel-T (brand name Provenge), helps direct the immune system to attack a typically incurable form of prostate cancer. The vaccine contains a patient's own cells, which have been "activated" in the lab through exposure to a prostate-cancer protein. Trials suggest the treatment extends patients' survival by a few months.

Scientists are investigating many more cancer vaccines, including some for brain cancer and skin cancer, in clinical trials. Different vaccines are at different points in the clinical trial process; some are still in early research, whereas others, such as Merck and Moderna's vaccine for melanoma, are in the final stage of clinical trials..

If current efforts to design cancer vaccines for secondary prevention are successful, Balachandran hopes that researchers could one day design cancer vaccines for primary prevention — stopping people from ever developing cancer in the first place. A vaccine for primary prevention would work more like a traditional shot for infectious diseases by blocking the condition from ever emerging.

"If we now know that the immune system can also recognize cancer, it should, in theory, be possible to develop a vaccine against cancer, like we have been able to do against pathogens," Balachandran said. "It's an exciting time for the field right now."

This article is for informational purposes only and is not meant to offer medical advice.

It's tough to resist scratching an itch — and there might be an evolutionary reason for that, a new study suggests.

People are typically advised not to scratch itchy skin — whether due to a bug bite or chronic condition — because too much abrasion can raise the risk of infection by injuring the skin and may worsen the itchiness. However, a study published Thursday (Jan. 30) in the journal Science found that some amount of scratching may be useful.

Turns out, scratching an itch increases inflammation and boosts the body's immune response at an itchy injury site, thus helping to ward off infection, the researchers discovered. The findings may help explain why scratching has been preserved across multiple species.

"If scratching an itch is bad for us, why does it feel so good?" study co-author Dr. Daniel Kaplan, a dermatologist and immunologist at the University of Pittsburgh, said in a statement. "Scratching is often pleasurable, which suggests that, in order to have evolved, this behavior must provide some kind of benefit."

Related: Inflammation is a 'mismatch between our evolutionary history and modern environment,' says immunologist Ruslan Medzhitov

To find out what that benefit might be, Kaplan and his colleagues bred mice that had certain itch-sensing neurons in their bodies deactivated. The researchers then dabbed an allergen on each mouse's ear to trigger an itchy sensation. They compared the allergic reactions in the modified mice to reactions in normal mice, some of which wore collars that prevented them from scratching, similar to the "cone of shame" that a dog might wear after a trip to the vet.

The normal mice without cones scratched their ears in response to the allergen and developed some swelling. The researchers found that this inflammation resulted from pain-sensing neurons releasing a substance that activates "mast cells," which act like alarms in the immune system. To trigger inflammation, these mast cells summon another type of immune cell called a neutrophil that helps corral the germs behind infections, among other roles.

Meanwhile, the mice with cones, along with the ones that couldn't feel the itch, developed much less swelling in their ears. This suggested that scratching was responsible for most of this inflammatory response.

Mast cells summon the body's defenses against infection, so scratching might protect against infection by activating these cells, the researchers proposed.

To test their hypothesis, the researchers exposed each mouse's ears to an itch-inducing substance followed by Staphylococcus aureus, a bacterial species that commonly causes skin infections. After a day, normal mice without cones had 10 times fewer S. aureus bacteria on their skin, compared to the mice with cones and those without itch-sensing neurons. This suggested that scratching boosted the mice's defenses against the bacteria.

The findings may offer some insight into why we itch in the first place.

"It's highly evolutionarily conserved," meaning it's a behavior widely seen on the tree of life and displayed across numerous species, said Liwen Deng, an immunologist at Harvard Medical School who was not involved in the new research. "But it just seems so damaging, and we really had no understanding of what could be helpful about it. So it really is one of the first studies to show that it could be a beneficial response," Deng told Live Science.

Despite these potential benefits, scratching does still have some negative effects, especially when it comes to chronic conditions. Scratching too much can worsen the inflammation to the point that it slows down the healing process. In short, you can have too much of a good thing.

"The finding that scratching improves defense against Staphylococcus aureus suggests that it could be beneficial in some contexts," Kaplan said. "But the damage that scratching does to the skin probably outweighs this benefit when itching is chronic."

This article is for informational purposes only and is not meant to offer medical advice.

In a first, scientists have designed immune cells that protect stem cell transplants from being rejected by the body — and they could someday open the door for a cure for diabetes.

The new cells, which were able to protect insulin-producing cells transplanted into mice, are an early "proof-of-concept," said study co-author Audrey Parent, an associate professor at the University of California, San Francisco (UCSF) Diabetes Center.

But if shown to be safe and effective in people, the designer cells could one day be used to protect transplanted tissues from attack, reducing or eliminating the need for drugs that suppress the immune system. That, in turn, could pave the way to a cure for diseases like type 1 diabetes.

In type 1 diabetes, immune cells, known as killer T cells, destroy pancreatic beta cells, which make insulin. In recent years, scientists have progressively inched closer to replacing destroyed beta cells with new cells derived from stem cells, which can be made to turn into any type of cell in the body.

Related: 'Like a reset button on a computer': Designer cells 'reboot' immune system in 3 different autoimmune diseases

In June, for instance, scientists reversed type 1 diabetes in a person by reprogramming their fat cells, while the Boston-based company Vertex Pharmaceuticals recently launched a pivotal, large-scale trial testing whether reprogrammed stem cells can eliminate the need for insulin in those with type 1 diabetes.

But before such stem-cell transplants can be widely used, scientists need to solve one big problem: In type 1 diabetes, killer T cells have been trained to target beta cells and have already destroyed those cells once. The transplanted cells need protection from this immune attack, so for now, patients need strong drugs that suppress the immune system. However, these drugs leave patients open to dangerous infections and are toxic to the kidneys and other organs.

To get around this problem, Parent and colleagues engineered T cells in the lab that protected the transplanted cells — known as a graft — from attack.

"We took an immune cell and changed the machinery inside it to make it a protective cell instead of a killer cell," Parent told Live Science. "And then we targeted it to the graft." Essentially, the designer cells act as bodyguards.

The bodyguards zero in on beta cells because they recognize a specific protein, called CD19, that the researchers added to the beta cells. When the bodyguard cells grab onto CD19, they then crank out a molecule that inhibits killer T cells.

The guards also make a protein that sops up an inflammatory chemical that normally helps activate killer T cells. This anti-inflammatory protein also tells the guards to replicate, creating a positive feedback loop that reinforces their ranks, Parent said.

To test their guards in a living organism, the researchers then took beta cells derived from stem cells and implanted them into mice. They then sent killer T cells to attack the transplanted beta cells. In one group of mice, they also injected their designer cells to defend the transplants.

In the mice not given designer cells, the killer cells quickly wiped out all the beta cells. But in the mice injected with designer cells, the transplants lived at least 35 days, and the mice were still producing insulin at that time, researchers reported in the study, published Thursday (Dec. 5) in the journal Science.

The results show it is possible to engineer T cells that can protect transplanted tissue, Parent said.

However, one challenge is finding a unique protein target to activate the designer cells, Parent said, as most potential targets are found on cells in multiple places in the body. That raises the chances that their designer cells will activate elsewhere in the body, beyond the transplants. That could pose a problem if, for instance, cells with the protein target become infected or cancerous, but can't be cleared because they are being protected by the guard cells. Transplant cells could be engineered to have a "kill" switch for those cases, but other cells in the body wouldn't have this switch.

Follow-up work may address this problem. For instance, the team could engineer an artificial target that would be found only on the transplanted beta cells and nowhere else, study co-author Wendell Lim, a biochemist and director of the UCSF Cell Design Institute, told Live Science in an email.

In a separate study, also published Thursday in Science, Lim and colleagues showed that similar designer T cells could target brain tumor cells while leaving healthy brain cells alone. The cells could also deliver anti-inflammatory chemicals to brain cells in mice with a disease similar to multiple sclerosis.

Looking forward, the team is also interested in seeing how this approach works against other autoimmune diseases fueled by inflammation, such as rheumatoid arthritis, as well as Crohn's disease and other inflammatory bowel diseases, Lim added. But it will be several years before these ideas can be tested in humans, he said.

"This work opens up a new avenue for treating inflammatory diseases in a targeted way," he said," but lots of pieces need to be put together and tested to come up with effective therapies."

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In an early-stage clinical trial, scientists used designer immune cells to "reboot" the immune systems of patients with various autoimmune diseases.

The trial used a form of chimeric antigen receptor (CAR) T cell therapy, which has become a mainstay treatment for blood cancers, like leukemia.

Only a few patients were included in this initial trial, and the trial was short — so it's too early to say whether this treatment works over the long term. But markers of disease in the patients' blood suggest the autoimmune processes had been shut down, at least for now.

If this therapy proves effective in larger, longer follow-up trials, it could change the way autoimmune diseases are treated.

"I think it will change the standard of care in lupus," said study co-author Dr. Georg Schett, vice president of research and head of the Department of Internal Medicine at Friedrich-Alexander University Erlangen-Nürnberg in Germany.

Related: In a 1st, scientists use designer immune cells to send an autoimmune disease into remission

Schett presented the trial's findings Sunday (Nov. 17) at the American College of Rheumatology meeting in Washington, D.C. The findings have not yet been peer-reviewed or published in a scientific journal.

Typically, lupus patients must take immune-suppressing treatments for life; by comparison, the new therapy requires only a single infusion. "If you have a single infusion and you don't need anything anymore, you're free," Schett told Live Science.

The trial was a "basket study," so named because patients with different conditions are tossed into one basket and all given the same treatment. In this case, the team treated 15 patients — 11 with severe lupus, three with systemic sclerosis and one with idiopathic inflammatory myopathies.

These autoimmune diseases have different symptoms, such as muscle weakness, thickened skin and kidney failure. However, all of them are caused by a subset of the body's B cells, a type of immune cell, going rogue and cranking out antibodies that target a person's tissue for destruction.

Normally, B cells work alongside T cells, which help call the B cells into action and can also kill cells directly. The most common type of CAR T cell therapy works by genetically tweaking a patient's T cells so they can spot and kill cancerous B cells more effectively.

In the new trial, the team gave each of the 15 patients with severe autoimmune disease one infusion of these designer immune cells. The CAR T cells then hunted and eliminated all of the body's B cells — both healthy ones and those driving autoimmune disease.

Seven days after this treatment, the designer cells had eliminated all of the B cells circulating in the patients' blood streams. By two months out, no B cells remained in any tissue, Schett said.

However, by three months after the infusion, the body had completely replenished the B cell population — and the B cells seemed to be healthy.

"It's like a reset button on a computer," Schett said. "You just take everything away, you shut it down, and then it reboots in a normal way and it doesn't have these [autoimmune] B cells anymore."

The trial was designed to test the safety of the new treatment, not how well it treats autoimmune disease. But "surrogate" markers of disease, such as the levels of tissue-targeting antibodies and T cells in the blood, appeared to be normalized.

In addition, all of the patients have been off their traditional treatments since their infusions — the longest for 11 months now.

One of the biggest worries with CAR T therapy used in cancer is "cytokine release syndrome," in which the body erupts into severe inflammation after treatment. That reaction did not seem to be a big issue here, the researchers reported.

As a follow-up, the team will evaluate the drug's efficacy in larger trials. They will also continue to follow these initial patients for longer periods, Schett said.

New research has revealed genetic features that may signal the onset of multiple sclerosis (MS) long before a person shows symptoms of the disease, scientists say.

MS is an autoimmune disease that causes inflammation in the brain and spinal cord. This inflammation damages myelin sheaths — the insulation that encases nerve cells' long "wires" — and leads to symptoms of pain, fatigue, numbness or weakness, as well as problems with vision or movement.

People with MS are known to have high levels of immune cells called cytotoxic T cells, which normally help kill cancer and cells infected by germs. In MS, however, these cells accumulate in areas with visible myelin damage, but the role the cells play in the disease has remained largely a mystery — until now.

In a study published Sept. 27 in the journal Science Immunology, researchers studied the T cells of 12 pairs of identical twins. In each pair, one twin had MS and the other did not. When one twin has MS, the second has about a 1 in 4 chance of developing the disease down the line. Thus, the second twin's T cells offer insight into the immune systems of people who are likely to eventually experience full-blown MS.

Related: Europeans' ancient ancestors passed down genes tied to multiple sclerosis, Alzheimer's risk

"Today, we have very good treatments for MS," study author Dr. Lisa Ann Gerdes, a neuroimmunologist at Ludwig Maximilian University of Munich, told Live Science. But people can't be treated until they are diagnosed — and the risk factors, triggers and earliest signs of MS are not completely understood.

"The MS Twin Study gives us a unique chance to look at patients with a prodromal [very early] stage of the disease, which is not possible in a real-world setting," Gerdes said. "Normally, if a patient has symptoms, the immune system has already entered the brain, so we are too late to see the main players driving inflammation in the beginning."

Notably, six of the twins without MS did have some inflammation in the central nervous system (CNS) that could be detected in tests but didn't yet cause any obvious symptoms.

The researchers looked at genes that were switched on in the twins' T cells by measuring RNA, a molecule that helps cells make proteins from DNA's blueprints. The analysis revealed that the T cells of people with either MS or CNS inflammation were more active, and triggered more immune signaling, than those in people with neither condition. In short, those T cells seemed especially reactive. The researchers also found more activation in genes that help keep T cells switched on.

By categorizing the hyperactive genes by disease stage, the researchers showed that the genes involved in T cell activation were most prominent in people who had CNS inflammation, but not full-blown MS. People with MS had more gene activity tied to helping T cells survive, move around the body, and call other parts of the immune system to attack.

Overall, the more advanced a person's disease stage was, the more T cells they had that showed these genetic changes. This lends weight to the hypothesis that these T cells drive inflammation in MS.

"Over and over again, studies demonstrate to us that the earlier we intervene in the process of inflammation and destruction of the nervous system, the greater the impact we have on our patients' disability outcomes," said Dr. David Duncan, a neurologist at Hackensack Meridian Health who was not involved in the research.

"Having insight into the earliest indicators of MS may help us make a diagnosis and initiate therapy long before any significant neurologic damage can occur," he said.

Related: 'Any protein you can imagine, it can deliver': AI will help discover the next breakthrough in RNA, says Nobel Prize winner Dr. Drew Weissman

To verify their findings, Gerdes and her colleagues went two steps further.

First, they analyzed T cells from another group of 17 people. Twelve had MS and the remaining five had a noninflammatory brain condition. In this group, people with MS had higher activation in genes associated with T cell activation, function and survival than the people who did not have MS.

Second, the researchers analyzed publicly available genetic data from more than 61,000 individual T cells sampled from brain tissue that had been damaged by MS. They looked to see which genes were overactive and found many of the same genes they had in their patient testing, along with others related to inflammation.

These analyses strengthen the findings, but even so, the researchers cautioned that their study included only a small number of people from similar backgrounds, especially in the twin cohort.

"It will be important to see these findings reproduced by other investigators and labs with larger sample sizes," Duncan told Live Science. "It's also important, as mentioned in the study, to evaluate other immune cell types that are involved in MS pathology."

Still, the researchers hope that understanding more about gene activity in the early stages of MS could lead to more accurate evaluations of who's at risk of MS, as well as faster diagnoses and more targeted treatments for the disease.

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A coveted research award that comes with a $250,000 prize is going to a scientist who helped uncover a protein's role in the human body's immune defenses.

Biochemist Zhijian "James" Chen, director of the Inflammation Research Center and a professor of molecular biology at the University of Texas Southwestern Medical Center, has won one of this year's Lasker Awards — biomedical-research prizes often called the "American Nobels."

Chen led work that resulted in the discovery of a critical enzyme — cyclic GMP-AMP synthase (cGAS) — that acts like a fire alarm in the body. But instead of being tripped by smoke, cGAS activates in response to the DNA of foreign invaders, such as viruses and bacteria. Prior to the discovery of cGAS, scientists didn't know how this DNA set off the innate immune system, the body's first line of defense against foreign substances.

Ilya Mechnikov, who won a Nobel in 1908, discovered phagocytosis, a phenomenon in which one cell gobbles up another. This is one way that immune cells rid the body of disease-causing bacteria. In his Nobel lecture, Mechnikov noted that bacterial DNA somehow awakens a "protective army of phagocytes" in the body — but at the time, no one knew how.

Related: Avi Wigderson wins $1 million Turing Award for using randomness to change computer science

Later research, conducted in the early 2000s, revealed that injecting cells with DNA drove a spike in interferons, immune signals that help stop infections. Scientists then uncovered a group of genes that enables the production of these interferons, which they dubbed "stimulator of interferon genes" (STING). STING does not directly sense foreign DNA, but the DNA somehow activates STING nonetheless.

Starting with a paper published in 2012, Chen and his collaborators finally started filling in the missing links in this chain of events. The first is cyclic GMP-AMP (cGAMP), a molecule that switches on STING when foreign DNA lurks in cells. The second is cGAS, the enzyme that enables the cells of mammals — including humans — to make cGAMP.

In the body's early warning system, cGAS is the alarm itself, which detects foreign DNA and calls in reinforcements in the form of cGAMP. In turn, cGAMP recruits the "fire brigade" — which in this case is the innate immune system, including the cells that gobble up invaders.

Chen's group later learned that this system detects not only DNA but also retroviruses, the group of viruses to which HIV belongs. These viruses contain RNA, a genetic cousin to DNA. HIV is a master of evasion when it comes to dodging the innate immune system — but when the virus is detected, it's cGAS that spots it.

Unfortunately, the cGAS alarm system isn't always helpful; in the context of some diseases, it can go haywire.

cGAS plays a role in autoimmune diseases, in which the immune system mistakenly attacks the body. cGAS detects DNA floating around in the fluid of a cell, which is usually a sign of infection. Our own human DNA is typically packaged neatly in compartments called the nucleus and mitochondria — but when a cell falls under stress, that DNA can leak out and end up elsewhere in the cell.

We have enzymes to help break down that escaped DNA, but in some people, these enzymes don't work well. And this deficiency, Chen and colleagues have found, can end up triggering the cGAS alarm system. This hints that cGAS could be key to reining in these harmful immune responses.

"cGAS has been implicated not only in autoimmune conditions, but in numerous inflammatory illnesses, including age-related macular degeneration and neurological disorders such as Parkinson’s disease, Alzheimer disease, and amyotrophic lateral sclerosis," the Lasker Award grantees wrote in a statement. "Calming the cGAS-cGAMP-STING pathway might therefore provide benefit across a broad span of ailments."

Chen was awarded the 2024 Albert Lasker Basic Medical Research Award.

Two other Lasker Awards were awarded this year — one for clinical research and one for public service. The first went to Joel Habener, Lotte Bjerre Knudsen and Svetlana Mojsov for their discovery and development of drugs that mimic the hormone glucagon-like peptide 1, such as Ozempic, for obesity treatment. The second went to Quarraisha Abdool Karim and Dr. Salim Abdool Karim, whose work has been instrumental in preventing and treating HIV.

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Some people just can't stop scratching after they're bitten by a mosquito — but not everyone gets itchy after a bug bite or similar allergy-triggering encounter. Now, new research in mice pinpoints differences in immune system activity that may determine whether you end up itchy.

The skin is densely populated with sensory neurons, which are nerve cells that detect changes in the environment and then trigger sensations, such as pain, in response. When a person encounters a potential allergen, like mosquito saliva, these neurons detect it and may trigger an itchy sensation in response. They also help activate nearby immune cells, which kick off an inflammatory reaction featuring swelling and redness.

Some people who are repeatedly exposed to an allergen can develop chronic allergic inflammation, which fundamentally changes the tissues where that inflammation is raging. For instance, the immune cells that respond to allergens can change the nerves' sensitivity, making them more or less likely to react to a substance.

"We all have sensory neurons, so we can all feel itchy — but not all of us get allergies, even though we're surrounded by the same allergens," senior study author Dr. Caroline Sokol, a professor of allergy and immunology at Harvard Medical School and Massachusetts General Hospital, told Live Science. "So what defines whose sensory neurons fire in response to allergens and whose don't?"

Related: Could allergies be 'deleted' someday?

To find out, Sokol and colleagues exposed mice to a chemical called papain, which causes an itchy sensation that makes mice scratch their skin. The different groups of lab mice in the study were missing different immune cells. The research, published Wednesday (Sept. 4) in the journal Nature, found that mice that lacked a specific type of T cell didn't scratch when they were exposed to papain.

The researchers wanted to find out how these cells, dubbed GD3 cells, drove sensory nerve responses. They grew GD3 cells in the lab and treated them with a chemical to make them release signaling molecules called cytokines. Then, they injected mice with normal immune systems with the cytokine-containing liquid the cells were grown in.

This treatment didn't trigger itchiness on its own. However, it did intensify the mice's scratching responses to a variety of allergens, including mosquito spit. This suggested that something released by GD3 cells hiked up the nerve-induced itching.

By comparing the chemicals secreted by GD3 cells with those from other immune cells in the central layer of the skin, the researchers discovered that only one factor was unique to the GD3 cells: interleukin 3 (IL-3), which is known to help regulate inflammation.

Only some sensory neurons responded to IL-3. Those that did respond became more likely to trigger an itch — a sign that the cytokine "primes" neurons to react to allergens.

In contrast, when the researchers removed the genes for IL-3 or its receptors — or removed the GD3 cells entirely — the mice could not initiate an allergic response. With further experiments, the researchers concluded that IL-3 activates two separate signals: one that promotes the nerve-driven itching and another that controls the immune side of the allergic response.

By releasing IL-3, the GD3 cells were "absolutely essential" for setting the threshold at which a sensory nerve would react to an allergen, Sokol said. This chain reaction involving IL-3 "may give us a new pathway to treat patients with chronic itch disorders," she added.

However, so far, the research has been conducted only in mice, so the researchers can't be certain that human cells will behave the exact same way. Although the mouse immune cells in the study have very similar genes and proteins as their human equivalents, Sokol emphasized that it's important to understand whether and how human T cells react to IL-3. That data is needed to translate the finding into itch treatments or ways to predict who might be at risk of allergies.

"We all have that friend who doesn't react to mosquito bites and the friend who looks horrific after a day outside," Sokol said. "We believe [the IL-3 pathway] is determining that in real time, because when we look at mosquito bite-induced itch — and the allergic immune response that follows — we see that it is completely dependent on the cells in this pathway."

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Defense systems found in all complex life on Earth came from "Asgard."

The ancestor of plants, animals and fungi evolved around 2 billion years ago, likely from a group of complex microbes called Asgard archaea — and we inherited two defense proteins that fight off viruses from those single-cell organisms, new research suggests.

"This study shows that if we want to understand the origins of our immune system, we need to include archaea, especially Asgard archaea, in the discussion," study first author Pedro Lopes Leão, a microbiologist at Radboud University in the Netherlands, told Live Science in an email.

The tree of life is broken up into three domains: Bacteria, Eukarya and Archaea. Bacteria are tiny, simple cells with no nucleus. Eukaryotes, by contrast, keep their DNA in a nucleus and have specialized "organelles," such as mitochondria and ribosomes, each of which performs specific functions. And then there are the microscopic-yet-complex archaea, which lack nuclei and organelles, but use energy in ways similar to eukaryotes.

"These microbes are super interesting because they are more like plants and animals (eukaryotes) than bacteria," senior study author Brett Baker, an associate professor of integrative biology and marine science at the University of Texas at Austin, told Live Science in an email.

Related: Meet LUCA, the 4.2 billion-year-old cell that's the ancestor of all life on Earth today

In 2015, scientists first described a newfound superfamily of archaea that bridged the gap between bacteria and eukaryotes. Named Asgard archaea because they were collected from a deep-sea hydrothermal vent in the Arctic known as "Loki's castle," these cells transformed our understanding of the evolution of complex life.

Follow-up research suggested that all eukaryotes evolved from Asgard archaea that lived around 2 billion years ago.

To understand more about how complex life first evolved, Baker's team sifted through thousands of genomes across the tree of life, identifying tens of thousands of "viral defense systems," or genes that code for proteins that fight viruses.

Of these, they zeroed in on genes that code for two classes of proteins: viperins and argonautes, that showed up across every domain of life.

In humans, viperins are part of the body's innate, or first-line, defense system. They were first described in humans and play a role in fighting off a wide array of viruses, from hepatitis C to HIV. They help keep viruses from making copies of viral proteins inside infected cells. Argonautes, on the other hand, were first found in plants that look like little squid, and stop viruses from making copies of themselves by chopping up their genetic material.

The genes for both classes of proteins were found across the huge array of life the team studied. But the genes were much more similar between archaea and eukaryotes than between bacteria and the other two domains.

In particular, the catalytic sites — key parts of the proteins that perform their essential functions — had changed very little over the 2 billion years since eukaryotes first evolved, the researchers reported.

The findings, published in July in the journal Nature Communications, suggest these two types of immune proteins originally came from an ancient Asgardian ancestor.

That the key sites on these proteins have evolved so little over the eons "speaks to the fact that they work well," Baker said.

As follow-up work, the team is looking for other defense systems in these microbes.

Researchers have developed an experimental HIV treatment that sustains itself in the body, with the goal of controlling virus levels for the long term after a single dose.

So far, the new treatment has been tested in monkeys, not people. But in the monkeys, it dramatically suppressed HIV for at least seven months. If the drug is approved for people someday, its protection might last years, said Adrian Wildfire, a virologist and drug development scientist who was not involved in the research.

"I suspect you'll see some decline in function [of the treatment] after five to seven years," Wildfire told Live Science. That represents a big jump from current treatment options.

About 40 million people worldwide are living with HIV, but only about three-quarters of them are currently receiving antiretroviral therapy, the standard treatment. A smaller percentage are virally suppressed, meaning the amount of HIV in their body has declined to extremely low levels.

Related: We could end the AIDS epidemic in less than a decade. Here's how.

Some people face difficulties obtaining an HIV diagnosis and therapy prescription; others may struggle to afford medication, tolerate its side effects, or remember to take the daily pills many treatment regimens require to keep the virus at bay. Some existing long-acting shots last weeks or months, but people typically need to reach suppression with pills before qualifying for the shots.

Complicating the challenge, the virus also evolves very quickly, meaning it can become resistant to treatments, especially if doses are missed. Without treatment, HIV rapidly destroys a key class of immune cell in the body, leaving the person vulnerable to cancers and infectious diseases. At this stage, the infection has progressed to acquired immunodeficiency syndrome (AIDS).

To overcome some of the issues with existing antiretrovirals, a group of researchers developed a new type of treatment: an engineered form of the virus that can outcompete HIV in the body.

In a study published Aug. 9 in the journal Science, the researchers used genetic engineering to create a version of HIV called a therapeutic interfering particle (TIP). This virus-like particle is designed not to harm its host, but it still replicates quickly. The idea is that, when injected into a person with HIV, the harmless TIP takes over, occupying and protecting cells that the virus would otherwise destroy.

To test that theory, the researchers developed a version of their TIP that resembled simian immunodeficiency virus (SIV), an HIV-like pathogen that infects monkeys. They injected it into six rhesus macaques (Macaca mulatta). After 24 hours, they infected the macaques with an aggressive virus with features of both SIV and HIV and tracked levels of infection for about seven months.

They found that the macaques that received TIPs had 10,000 times lower levels of virus than four infected monkeys that hadn't received the shot. The TIP-injected monkeys also had stronger immune responses and no evidence of inflammation. The untreated monkeys had quickly developed severe illnesses.

Related: People on HIV meds have 'almost zero' chance of spreading virus via sex once levels are low

As designed, the TIPs continued to replicate in the macaques' bodies throughout the entire study period, hinting that long-lasting treatment may be possible.

"These primate studies show the promise of a single-dose TIP intervention and are a strong indicator of efficacy in human trials," senior study author Leor Weinberger, a professor of pharmaceutical chemistry, biochemistry and biophysics at the University of California, San Francisco, said in a statement.

The researchers also applied their TIPs to lab mice with human immune cells and to blood cells from people living with HIV. In both cases, the TIPs outcompeted HIV and suppressed the infection.

"You're reducing viral replication a lot, which could allow people to live with fewer symptoms because far fewer of their T cells are being destroyed," Wildfire told Live Science. But he doesn't think the treatment will last indefinitely.

Because of their similarity to unmodified viruses, TIPs stimulate various immune cells in the body that can eventually become exhausted by this. This opens the door for more TIPs and HIV to enter cells — but since HIV continually evolves, this exhaustion could theoretically allow HIV to gain a foothold over TIPs.

"So what's the outlook on this? Relatively positive in the short term, but I think more work is needed in the long run," Wildfire said.

The researchers have not yet tested whether this new treatment could replace antiretroviral drugs for people who are already living with well-controlled HIV. Their next step is to test this idea in macaques, after which they hope to embark on human clinical trials. The end goal is to offer new options for HIV treatment so people won't have to take medications continually for the rest of their lives.

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For the first time, scientists have bred mice with fully fledged human immune systems. The researchers say these human-like animals will enhance drug development.

When faced with an infection, these "humanized" mice produce immune cells that mimic the structure and diversity of the immune cells made by humans. When injected with a chemical that triggers widespread inflammation in the body, the mice develop a version of the autoimmune disease lupus that closely resembles that seen in humans, the researchers discovered. 

The scientists described their findings in a paper published June 25 in the journal Nature Immunology. 

These are not the first humanized mice ever bred — the lab animals are staples in research as they enable scientists to study features of the human immune system inside a living animal. This is helpful for testing the safety and effectiveness of new drugs, as well as vaccines against infectious diseases, before they are trialed in humans. 

Related: New immunotherapy could make blood more 'youthful,' mouse study hints

However, for years, researchers have struggled to create humanized mice that accurately respond to infection in the same way that humans do. Previous attempts have resulted in approximations of the human immune system, but these are missing certain human features, the team behind the new paper said in a statement. 

To develop a better humanized mouse, the researchers first bred mice that had been genetically modified to have a weakened immune system. When the mice were around 1 to 2 days old, the team injected human stem cells into the animals' hearts. The stem cells, which had been extracted and purified from umbilical cord blood, were capable of becoming any type of immune cell. 

The animals' hearts then pumped the stem cells into the soft, spongy tissue within the mice' bones, known as bone marrow, which is where immune cells are normally produced. Because the mice were immunodeficient, the human stem cells could easily set up camp in the bone marrow. 

After a few weeks, the team introduced a human version of the sex hormone estrogen into the mice. This hormone is known primarily for its role in promoting female sexual and reproductive development, but it also plays a big part in molding immature stem cells into mature, specialized immune cells. 

Once imbued with human estrogen, the mice began to make a plethora of human immune cells. These included T cells, which directly attack germs, and B cells, which produce bug-busting antibodies that help mark pathogens for destruction. 

To see how the humanized mice reacted to a vaccine, the team injected the animals with the COVID-19 vaccine made by Pfizer-BioNTech. In response, the mice produced human antibodies against the coronavirus, SARS-CoV-2. Similarly, when exposed to proteins from Salmonella typhi bacteria, the bug behind typhoid fever, the mice made antibodies against the pathogen. 

The new mouse model could become a valuable tool for biomedical research, the team said. In particular, these mice will be useful for vaccine development, said Dr. Paolo Casali, a co-senior study author and professor of medicine at the University of Texas.

As the new mice have a "100% human immune system," researchers can use them to test how vaccines will behave in a living body. In the early stages of research, such tests can't be done in humans for ethical reasons, Casali told Live Science.

The mice could also be used to develop new therapies that work by tweaking the activity of the immune system, such as checkpoint inhibitors for cancer, he said. These drugs help the immune system to better target cancer cells for destruction. 

Using mice that have a human immune system could help facilitate this kind of research, potentially even removing the need to use non-human primates, the team said in the statement. 

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Immune signatures in the blood may flag if someone has ovarian cancer up to four years earlier than conventional methods used to diagnose the disease, new research suggests. 

Ovarian cancer is one of the deadliest cancers, with a five-year survival rate of less than 51%. Around 70% of ovarian cancer patients have high-grade ovarian cancer (HGOC), in which cancerous cells look particularly abnormal and are more likely to grow and spread than low-grade cancers. 

As with many cancers, early diagnosis and treatment — such as with surgery and chemotherapy — are key to longer survival. If this type of cancer is localized — that is, limited to the ovaries or the fallopian tubes — around 93% of patients are expected to survive for five or more years after diagnosis.  

Unfortunately, most patients are not diagnosed with HGOC until the cancer is at an advanced stage, meaning it has spread to somewhere else in the body. In these cases, the five-year survival rate may be as low as 31%. 

Related: Gen Xers will have higher cancer rates than boomers, study forecasts

One reason for this is that HGOC doesn't have specific symptoms in the early stages of the disease. Also, during this time, tumors are very small and conventional biomarkers — such as the CA-125 blood test, which detects raised levels of a cancer-related protein — are not sensitive enough to detect them. 

However, the findings of a new study, published June 14 in the journal Cell Reports Medicine, may help doctors diagnose ovarian cancer much sooner, allowing for earlier treatment before the cancer has spread and, potentially, longer survival. 

In the study, researchers discovered a blood-based immune biomarker that they say could be used to detect HGOC up to four years before most cases are currently diagnosed. 

They uncovered this biomarker after analyzing blood samples taken from 466 patients who, within five years of their sample being drawn, went on to be diagnosed with ovarian cancer using conventional clinical tests. 

Specifically, the team noticed strong differences in the numbers of immune cells called T cells in their blood that were primed to recognize and attack cancer cells, compared with those found within the blood of a comparison group of women who did not go on to develop cancer. 

These signals could be detected two to four years before diagnosis and show that the immune system is actively fighting the disease, the study authors said. 

The research is still in its early stages. However, this "unprecedented discovery" could one day inform the development of new tests that detect this newly identified biomarker, the team said. 

"Early detection of ovarian cancer could mean the difference between life and death for millions of women," Bo Li, co-senior study author and a researcher at the Children's Hospital of Philadelphia's Center for Computational and Genomic Medicine, said in a statement. 

"We believe our findings can be a gamechanger, providing insights for the development of an immune-based biomarker to detect early-stage ovarian cancers."

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The COVID-19 pandemic drastically reduced people's in-person interactions with others as events were canceled and people limited their excursions, and many also practiced social distancing and masked up if they did go out. These moves were intended to control the spread of the disease and were shown to help flatten the curve.  

However, some concerns have been raised about the potential impact of these actions on children's immune systems, and namely, kids' ability to fight infections. But did COVID "lockdowns" and other pandemic-related restrictions actually stunt kids' immune systems? 

On that front, parents should not fear, experts told Live Science. Social distancing did not permanently stunt children's immune systems. Rather, it just delayed young children's exposure to various germs.

"During the COVID lockdown, our children were exposed to far fewer pathogens than they typically are in a normal year," Dr. Sarah Nicholas, an assistant professor of pediatrics-allergy and immunology at Baylor College of Medicine in Texas, told Live Science. 

Related: Master regulator of inflammation found — and it's in the brain stem

Examples of common respiratory viruses that children may be exposed to include respiratory syncytial virus (RSV); the flu, or influenza; and human metapneumovirus, as well as various viruses that cause the common cold. After such an infection, the body builds up its immune defenses so that it can tackle these pathogens if it encounters the same ones again. 

Social distancing reduced not only the spread of COVID-19 but also that of other respiratory viruses, which tend to spread in similar ways. When these restrictions were lifted, the viruses were free to circulate in the population again. In addition, viruses responsible for causing other types of disease, such as viral gastroenteritis or stomach flu, also began spreading again. 

As social distancing behavior waned, toddlers who had never caught these viruses were suddenly playing "catch-up" with their immune systems, Dr. James Antoon, an assistant professor of pediatrics at Monroe Carell Jr. Children's Hospital at Vanderbilt in Tennessee, told Live Science. Consequently, many children became sick at the same time, leading to a surge in hospitalizations, he said. 

In the spring and summer of 2021, there was an unusual surge in RSV cases in the U.S.; the virus's transmission normally peaks in the winter. There was also a particularly large spike in cases of RSV between 2022 and 2023 that inundated many hospitals in the country. 

Although this resurgence was notable, several studies suggest that the severity of children's illnesses did not rise as COVID-19 restrictions relaxed. In other words, although case numbers rose, on a whole, children were no less able to combat these infections than kids their age had been before the pandemic. 

And while social distancing reduced children's exposure to germs, most children likely still underwent routine vaccination regimens during the pandemic, Dr. Janko Nikolich, a professor of immunobiology at the University of Arizona, told Live Science. These vaccines help prime children's immune systems against many major pathogens that are harmful to their age group. Thus, their immunity would be ready for action as social distancing eased. 

Notably, though, there was a dip in children's routine vaccinations during the pandemic, and many are still catching up to this day. 

"We know that with COVID and with flu that vaccination is absolutely the best way to prevent poor outcomes, hospitalization and complications from these viruses," Antoon said. "So if your child is eligible for some of these vaccines, it's advantageous to get them."

Parents should know that children's immune systems are generally robust, regardless of whether they lived through pandemic lockdowns, Dr. Dean Blumberg, chief of the Division of Pediatric Infectious Diseases at UC Davis Health, told Live Science. "The difference is that there were atypical patterns of exposure and infection" during and immediately after the pandemic, he said. 

"We're hopeful that kids are caught up now and going forward we shouldn't see these atypical patterns of infection," he said. 

Importantly, the pandemic highlighted the impact that basic public health measures can have in preventing the spread of harmful viruses, Antoon said. In daily practice, such measures can include staying home, social distancing and masking when you're sick. 

"Those are measures that are really easy to do and we can continue moving forward in a reasonable way," he said. 

This article is for informational purposes only and is not meant to offer medical advice.

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Scientists have found a master regulator of inflammation — and it's in the brain stem. 

New research in mice has revealed that the neurons in the brain stem act like a thermostat, ramping up or down inflammation in response to signals sent by the vagus nerve, which connects the brain to other organs in the body. 

In the early stages of an infection, these neurons might encourage a helpful, proinflammatory response to thwart invading pathogens. However, once an infection is cleared, the neurons tamp down this response to prevent unwanted damage to healthy cells. Researchers described this feedback system in a new study published May 1 in the journal Nature. 

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower

If a similar feedback loop is found in humans, scientists could one day identify drugs that regulate it. For instance, drugs that target this brain stem thermostat could be used to reduce inflammation in diseases where it goes out of whack, such as autoimmune diseases, the researchers said. 

"If we can come up with small molecules that go into these neurons and turn them on, now you may have a way of regulating the circuit and therefore changing the way they are modulating body immunity and the inflammatory state," Charles Zuker, head of the laboratory where the study was carried out and a professor of biochemistry, molecular biophysics and neuroscience at Columbia University, told Live Science. 

The brain stem connects the main part of the brain, the cerebrum, to the cerebellum and the spinal cord, and it regulates key involuntary functions such as breathing and heart rate. Researchers already knew that the brain and the immune system communicate closely with one another, but the role of the brain stem in that process wasn't clear.

Scientists also knew that the vagus nerve plays a key role in inflammation; stimulating the nerve has been shown to work in several inflammatory conditions, including inflammatory bowel disease (IBD) and rheumatoid arthritis. However, exactly how all these players interact wasn't clear. 

To elucidate that relationship, in the new study, Zuker and colleagues stimulated an infection in mice using bacterial molecules that normally trigger an inflammatory response. 

The molecules triggered the vagus nerve to send signals to neurons in the caudal nucleus of the solitary tract (cNST) in the brain stem.

In a separate experiment, quieting these cNST neurons triggered a heightened inflammatory response, causing the body to crank out three times more pro-inflammatory molecules and three times less anti-inflammatory molecules than is typical in healthy mice.

Stimulating these neurons, meanwhile, had the opposite effect — levels of pro-inflammatory molecules declined by nearly 70% while anti-inflammatory molecules soared by almost 10-fold. This suggests that cNST neurons may control the body's inflammatory response to infection, the team said. 

Despite these promising initial findings, many questions remain. For instance, more research will be needed to understand the nature of the signals that pass from the brain stem to immune cells in the rest of the body, Tamar Ben Shaanan, a postdoctoral scholar in microbiology and immunology at the University of California, San Francisco, who was not involved in the research, told Live Science in an email. 

It would also be important to decipher how the complex immune "picture" is being seen in the brain, said Jonathan Kipnis, a professor of pathology and immunology at Washington University School of Medicine in St. Louis, who was also not involved in the research. 

For example, future research could investigate whether the brain knows that an infection has taken place, can identify which exact infection it is or develop memory of it in case of subsequent reinfection, he told Live Science in an email.  

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As a child, you may have been told that playing outside in the dirt is good for you because it strengthens your immune system. But is there any evidence to back this claim? 

In short, yes — several studies suggest that early exposure to dirt may reduce kids' risk of developing allergies and autoimmune conditions. In other words, it may guard against conditions in which the immune system unhelpfully reacts to allergens or to the body's tissues.

As a child's immune system develops in the early years of life, the army of protective cells within the body have to learn how to distinguish between the body's own cells and foreign substances that are either harmless or disease-causing, such as bacteria and viruses. It must learn to spot the disease-causing pathogens in order to attack them. 

Related: What do some allergies last a lifetime? Newly described immune cells to blame

It turns out that the molecular signals that drive the expansion of this regulatory arm of the immune system mainly come from microbes in the gut, Graham Rook, a professor emeritus of medical microbiology at University College London, told Live Science. This collection of microbes is called the "gut microbiome" and is essential to our health. For instance, some of these microbes help produce vitamins that we need to live, and they help us digest our food. 

The first year of life is crucial to the microbiome's development. Babies receive bacteria as they pass through the birth canal, if they're born vaginally, and from milk if they're breastfed. As children grow, they are steadily exposed to microbes from a wide array of sources. 

A theory called the "old-friends hypothesis" suggests that, the greater the range of microbes we're exposed to in early childhood, the more diverse our microbiomes will be and thus the better our immune systems will recognize friend from foe. The term "old friends" refers to helpful, or "commensal," microbes that live on and in the body without harming a person's health.

This theory, proposed by Rook in 2003, is similar to the more widely known hygiene hypothesis, which suggests that a lack of early exposure to germs makes people more prone to immune conditions. Multiple studies, for instance, have demonstrated a link between growing up on a farm or in a household with pets and having a lower likelihood of children developing allergies, compared with kids in urban or pet-less environments. 

However, the old friends hypothesis stresses the importance of being exposed to commensal microbes in early life, as opposed to infectious pathogens. This idea is backed by research: several studies in Europe suggest early exposure to germs does not guard against the development of allergies. Another critique of the hygiene hypothesis is that it downplays the importance of good hygiene to preventing disease, pushing the idea we've become "too clean," Rook and colleagues argued in a 2016 review. 

The old friends hypothesis, on the other hand, could help explain why antibiotic overuse in early life, which can wipe out much of the gut microbiome, and cesarean deliveries, which don't expose newborns to vaginal bacteria, have been tied to an increased risk of allergies. 

A trial in Finland looked at whether city kids' immune systems could be bolstered with grass and soil that had been taken from the forest floor. They found that, within a month, children who played in the dirt had a more diverse collection of harmless bacteria on their skin and more immune-regulatory cells and signaling molecules in their blood than those who played on gravel playgrounds. This hints that exposure to bacteria within dirt could help the immune system mature, theoretically reducing the chances of it becoming overactive. 

Similarly, a Swedish study published in 2024 found that children who either grew up on dairy farms or had pets had lower rates of allergies than those who didn't. They also had more harmless bacteria in their guts, so the study authors concluded that the two phenomena may be linked.

While the microbiome is important, there are many other factors that affect someone's risk of developing allergies, including their genetics, Dr. Robert Wood, a professor of pediatrics at Johns Hopkins Medicine in Baltimore, told Live Science. As a general message, though, children should be encouraged to go outside and play in the dirt, he said. 

However, scientists' current understanding of risk factors for immune conditions can't always be translated into practical advice. For instance, if you have a dog, you may have a somewhat lower chance of developing allergies than a pet-less person — but you can't tell somebody to get a dog as a guaranteed way to prevent allergies, Wood said.

Dirt in heavily polluted areas can also be unhealthy for kids, as it could contain harmful contaminants, he noted. This clearly wouldn't be the sort of dirt that you'd want your child to be exposed to. And because dirt can contain potentially harmful chemicals, such as lead, as well as parasites, care should be taken to stop children from inhaling or eating it.

Editor's note: This article was updated on Nov. 28, 2024 to include information about the Swedish study. The article was originally published on April 2, 2024.

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Scientists reversed some signs of immune aging in mice with a new treatment that could one day potentially be used in humans. 

The new immunotherapy works by disrupting a natural process by which the immune system becomes biased towards making one type of cell as it ages. 

The mouse study is an "important" proof-of-concept, but it's currently difficult to gauge the significance of the findings, Dr. Janko Ž. Nikolich-Zugich, a professor of immunobiology at the University of Arizona who was not involved in the research, told Live Science in an email. More work is needed to see how well the therapy shifts the immune system into a more youthful, effective state.

All blood cells, including immune cells and the red blood cells that carry oxygen around the body, start life as hematopoietic stem cells (HSC) in the blood and bone marrow, the spongy tissue found within certain bones. HSCs fall into two main categories: those destined to become so-called myeloid cells and those that will develop into lymphoid cells. 

Myeloid cells include red blood cells and immune cells belonging to our broadly reactive first line of defense against pathogens, including cells called macrophages that trigger inflammation. Lymphoid cells include cells that develop a memory of germs, such as T and B cells. 

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower

As we age, the HSCs slated to become myeloid cells gradually increase in number and eventually outnumber the lymphoid stem cells. This means we can't respond to infections as well when we're older as when we're young, and we're more likely to experience chronic inflammation triggered by increasing levels of myeloid cells that trigger inflammation.

In the new study, published Wednesday (March 27) in the journal Nature, scientists developed an antibody-based therapy that selectively targets and destroys the myeloid HSCs, thus restoring the balance of the two cell types and making the blood more "youthful." The antibodies latch onto the targeted cells and flag them to be destroyed by the immune system. 

The authors injected the therapy into mice aged 18 to 24 months, or roughly the equivalent of being between 56 and 69 years old as a human. 

They then extracted HSCs from the mice after treatment and analyzed them, revealing the rodents had a smaller percentage of the myeloid HSCs than untreated mice of the same age. 

This effect lasted for two months. Compared with untreated mice, the treated mice also produced more naive T cells and mature B cells. These cells can go on to form memory cells, which are directly involved in the immune attack; in the case of the B cells, they can form antibody-producing plasma cells. 

"Not only did we see a shift toward cells involved in adaptive immunity, but we also observed a dampening in the levels of inflammatory proteins in the treated animals," Dr. Jason Ross, lead study author and postdoctoral researcher at Stanford University, said in a statement. Specifically, the researchers saw that the levels of one proinflammatory protein fell in the treated mice. This protein, called IL-1beta, is mainly made by myeloid cells. 

Eight weeks post-treatment, the researchers vaccinated the mice against a virus they'd never been exposed to before. The mice that had received the immunotherapy had more apt immune responses to vaccination than the untreated mice, producing more T cells against the germ. 

"We believe that this study represents the first steps in applying this strategy in humans," Ross said. However, other experts have cautioned against jumping to conclusions.  

Nikolich-Zugich noted that, although the researchers measured changes in the numbers of naive T cells in the mice, they didn't look at the function of the organ that makes them: the thymus. The team also saw reductions only in IL-1beta and not other inflammatory proteins. They also didn't test whether the mice's baseline immunity to new infections could be improved with this therapy, without vaccination, he said. 

Furthermore, the study didn't consider potential long-term side effects of the treatment, such as anemia, or a deficiency in red blood cells, said Dr. Ilaria Bellantuono, a professor in musculoskeletal aging at the University of Sheffield in the U.K. who was not involved in the research.

Although an "interesting" study, more work is needed to understand whether it can bring "meaningful changes" in the immune system, Bellantuono told Live Science in an email, whether that of mice or humans. 

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The pursuit of a cure for Alzheimer's disease is becoming an increasingly competitive and contentious quest with recent years witnessing several important controversies.

In July 2022, Science magazine reported that a key 2006 research paper, published in the prestigious journal Nature, which identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer's, may have been based on fabricated data.

One year earlier, in June 2021, the U.S. Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment for Alzheimer's, even though the data supporting its use were incomplete and contradictory. Some physicians believe aducanumab never should have been approved, while others maintain it should be given a chance.

With millions of people needing an effective treatment, why are researchers still fumbling in this quest for a cure for what is arguably one of the most important diseases confronting humankind?

Escaping the beta-amyloid rut

For years, scientists have been focused on trying to come up with new treatments for Alzheimer's by preventing the formation of brain-damaging clumps of this mysterious protein called beta-amyloid. In fact, we scientists have arguably got ourselves into a bit of an intellectual rut concentrating almost exclusively on this approach, often neglecting or even ignoring other possible explanations.

Regrettably, this dedication to studying the abnormal protein clumps has not translated into a useful drug or therapy. The need for a new "out-of-the-clump" way of thinking about Alzheimer's is emerging as a top priority in brain science.

My laboratory at the Krembil Brain Institute, part of the University Health Network in Toronto, is devising a new theory of Alzheimer's disease. Based on our past 30 years of research, we no longer think of Alzheimer's as primarily a disease of the brain. Rather, we believe that Alzheimer's is principally a disorder of the immune system within the brain.

The immune system, found in every organ in the body, is a collection of cells and molecules that work in harmony to help repair injuries and protect from foreign invaders. When a person trips and falls, the immune system helps to mend the damaged tissues. When someone experiences a viral or bacterial infection, the immune system helps in the fight against these microbial invaders.

The exact same processes are present in the brain. When there is head trauma, the brain's immune system kicks into gear to help repair. When bacteria are present in the brain, the immune system is there to fight back.

Alzheimer's as autoimmune disease

We believe that beta-amyloid is not an abnormally produced protein, but rather is a normally occurring molecule that is part of the brain's immune system. It is supposed to be there. When brain trauma occurs or when bacteria are present in the brain, beta-amyloid is a key contributor to the brain's comprehensive immune response. And this is where the problem begins.

Because of striking similarities between the fat molecules that make up both the membranes of bacteria and the membranes of brain cells, beta-amyloid cannot tell the difference between invading bacteria and host brain cells, and mistakenly attacks the very brain cells it is supposed to be protecting.

This leads to a chronic, progressive loss of brain cell function, which ultimately culminates in dementia — all because our body's immune system cannot differentiate between bacteria and brain cells.

When regarded as a misdirected attack by the brain's immune system on the very organ it is supposed to be defending, Alzheimer's disease emerges as an autoimmune disease. There are many types of autoimmune diseases, such as rheumatoid arthritis, in which autoantibodies play a crucial role in the development of the disease, and for which steroid-based therapies can be effective. But these therapies will not work against Alzheimer's disease.

The brain is a very special and distinctive organ, recognized as the most complex structure in the universe. In our model of Alzheimer's, beta-amyloid helps to protect and bolster our immune system, but unfortunately, it also plays a central role in the autoimmune process that, we believe, may lead to the development of Alzheimer's.

Though drugs conventionally used in the treatment of autoimmune diseases may not work against Alzheimer's, we strongly believe that targeting other immune-regulating pathways in the brain will lead us to new and effective treatment approaches for the disease.

Other theories of the disease

In addition to this autoimmune theory of Alzheimer's, many other new and varied theories are beginning to appear. For example, some scientists believe that Alzheimer's is a disease of tiny cellular structures called mitochondria — the energy factories in every brain cell. Mitochondria convert oxygen from the air we breathe and glucose from the food we eat into the energy required for remembering and thinking.

Some maintain that it is the end-result of a particular brain infection, with bacteria from the mouth often being suggested as the culprit. Still others suggest that the disease may arise from an abnormal handling of metals within the brain, possibly zinc, copper or iron.

It is gratifying to see new thinking about this age-old disease. Dementia currently affects more than 50 million people worldwide, with a new diagnosis being made every three seconds. Often, people living with Alzheimer's disease are unable to recognize their own children or even their spouse of more than 50 years.

Alzheimer's is a public health crisis in need of innovative ideas and fresh directions. For the well-being of the people and families living with dementia, and for the socioeconomic impact on our already stressed health-care system coping with the ever-escalating costs and demands of dementia, we need a better understanding of Alzheimer's, its causes, and what we can do to treat it and to help the people and families who are living with it.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.

"It took the rug right out from under my life. I went to work that Friday in August; I never went to work a day since, and it'll be 10 years this August."

Those are the words of Jennifer Caldwell, whose life suddenly changed trajectory on an autumn weekend in 2014. Having wrapped up her workweek as a clinical research coordinator the day before, she spent Saturday swimming in her neighborhood pool. But later that day, abdominal pain and violent vomiting episodes sent her to urgent care and then to the ER. 

She had colitis, or inflammation of the colon, caused by Clostridioides difficile bacteria, which her doctors treated. However, the infection triggered a debilitating condition that Caldwell lives with to this day: myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. More than 4 million U.S. adults reported having the condition in 2022, but there are not yet any approved treatments for this typically lifelong disease.

Scientists and doctors once thought ME/CFS was a psychological disorder rather than a physical ailment, but over time, data emerged to show that it's in fact a biological illness. Now Caldwell, along with 16 other people with ME/CFS, is helping unravel the biological causes of this understudied condition.

She and the others contributed a trove of data to a landmark National Institutes of Health (NIH) study, published Wednesday (Feb. 21) in the journal Nature Communications, which reveals distinct differences between the bodies of people with ME/CFS and those without it. Differences in brain function and the immune system stand out, in particular, and the data could someday lead to treatments.

Those treatments may not come for a while yet, though, and just this initial study took many years, in part due to disruptions caused by the COVID-19 pandemic.

Related: What ME/CFS can teach us about 'long COVID'

"It was very ambitious to try and throw every test they could think of at a group of patients, and at the time, I thought it was a good idea for a study," said Brian Vastag, one of the study participants, an ME/CFS advocate and a former science reporter for The Washington Post. "But in the end, I just feel so ambivalent about it because it took so long," he told Live Science.

Caldwell, who first contributed data to the study in 2017, told Live Science that she hopes the long-awaited paper helps to validate ME/CFS in the eyes of doctors and the public. "General public has no clue, and 95% of the doctors I've seen … no clue what ME/CFS is," she said.

But both Caldwell and Vastag expressed hope that the study leads to treatments.

"Way back in 2016, when [then-NIH Director] Dr. [Francis] Collins announced this initiative, he did promise the patient community that the study that's being published would just be the first stage," Vastag said. "So they need to follow through, they need to start trials — that would give me some hope."

What the study found

The symptoms of ME/CFS affect many systems in the body and most often set in after an infection caused by bacteria or viruses. The new study focuses on people with this type of post-infectious ME/CFS. 

ME/CFS symptoms and their severity can vary among people, but they include losing the ability to engage in physical activity, as well as experiencing thinking problems and sudden dips in blood pressure when changing position. Due to a phenomenon called "post-exertional malaise," the symptoms can suddenly get worse after physical or mental exertion, so people with the condition have to carefully pace themselves to avoid crashing.

Notably, these symptoms often overlap with those of long COVID, a chronic condition that can emerge after a COVID-19 infection and that research suggests frequently shares both clinical and biological features with ME/CFS. Indeed, in the early days of the pandemic, researchers and advocates predicted that the novel coronavirus might trigger the syndrome. 

Because of this overlap, "whatever we learn from long COVID will be applicable to the ME/CFS and vice versa," senior study author Dr. Avindra Nath, clinical director of the NIH's National Institute of Neurological Disorders and Stroke, told Live Science.

To uncover potential causes of ME/CFS, the NIH recruited 17 people with the syndrome and 21 volunteers without the condition, for comparison. Each person underwent an extensive array of tests, including brain scans, cognitive exams, sleep tests, blood draws, spinal taps and exercise challenges.

The brain scans measured the flow of oxygenated blood through the brain while participants performed a grip-strength test. These tests revealed that ME/CFS patients showed low activity in a part of the brain called the temporal-parietal junction (TPJ) compared with the comparison group. This brain region checks whether a person is successfully performing an action they're attempting to execute, and it's part of a larger feedback loop that helps control the effort a person exerts and their sense of fatigue. 

"It's a functional suppression; it's not a structural damage," Nath said. In other words, the difference seen in the TPJ is a difference in brain activity rather than damage to the brain's physical structure.

Through the spinal taps, the researchers linked ME/CFS to low levels of chemical messengers that are involved in controlling involuntary bodily functions, such as heart rate and blood pressure. These low numbers indicate dysfunction in a hormone-making gland called the hypothalamus, and they also help explain the low TPJ activity. In addition, they hint at why, in people with ME/CFS, the body can't easily adjust its functions to contend with effortful or stressful situations, Nath said.

Related: 'Long flu' is real, and we've likely 'ignored it for a long time'  

The immune systems of ME/CFS patients also differed from those of the volunteers without the syndrome. For example, they showed signs of T-cell exhaustion, in which immune cells' activity becomes suppressed after they're active for too long. They also carried more naive B cells, immune cells that are broadly reactive and can fight multiple perceived threats to the immune system rather than being trained to attack one foe.   

ME/CFS patients' immunity not only differed from that of healthy controls but also differed depending on participants' sex, Nath noted. The study found key distinctions in gene activity, molecular signs of inflammation and immune cell populations between male and female participants. For example, the gene activity of males' T cells appeared disrupted in a way that would affect the cells' ability to activate; meanwhile, female participants carried B cells whose ability to proliferate had been hampered.

"That, I think, is an important part to take forward from this study," Nath said.

What's next?

The results paint a picture of distinct changes in the body and brain and overworked immune systems that drive perpetual inflammation. As Caldwell described it, "It's not good to have your immune jacked up constantly for years. But mine has been, and so your body is constantly battling things that there's no need to be battling." This was previously thought to be a potential cause of ME/CFS, but the new study helps explain what's happening at the level of cells and molecules. 

What's more, NIH data published last year suggest that the cells of people with ME/CFS can't easily make new fuel after using it up on a given activity. So the syndrome also may be tied to dysfunction in mitochondria, the powerhouses of cells.

But even with the newly available data, more steps remain before treatments can be developed.

"We need to validate these findings, but they can be done in the context of a clinical trial," Nath said. There's now enough data to start pinpointing potential therapies, narrowing down which populations of ME/CFS are likely to benefit, and then testing these in trials. Once selected, multiple drugs could even be tested in the same trial, with, for example, four groups receiving different treatments and one receiving a placebo. This could speed up the process, Nath suggested. 

One possible treatment proposed in the study is an existing cancer therapy called immune checkpoint inhibitors. The idea is that ME/CFS patients might have lingering bits of viruses or bacteria that are constantly setting off their immune systems, exhausting their cells. The checkpoint inhibitors could release the brakes of those exhausted T cells, theoretically enabling them to finish the job and clear away the substances continually triggering the immune system. 

As these trials get off the ground, ongoing long-COVID treatment trials — including one being led by Nath to test antibodies called IVIG — could also provide hints as to what to try in ME/CFS patients, and vice versa. Vastag argues that the research efforts should be combined, because he says many cases of long COVID are post-infectious ME/CFS.

Although the clinical research is often very slow, he said, scientists need to urgently bring people solutions for ME/CFS.

"One thing I want people to know is that this illness is a matter of life and death," he told Live Science. "A lot of patients, they don't have any hope that they will ever get better, and they end up ending their lives." Vastag's life partner, ME/CFS advocate Beth Mazur, died in December 2023 after living with the condition for 15 years, and through the years, Vastag has known others with the disease who died by suicide. It's with that in mind that he hopes the NIH will launch treatment trials expeditiously.

Caldwell, too, hopes trials will start soon. "I would be [the] first one in line because my life — my quality of life is very poor," she said. She spends 90% of her life in bed, leaving the house only to see the doctor or, rarely, to catch one of her daughter's basketball games, she said.

"My biggest reason for wanting to get better is for her," Caldwell said. "There's things for long COVID that they're trying that I would give anything for them to try it for me."

Warm weather will soon grace the U.S., replacing the short, cold days of winter — but it will also usher in an onslaught of seasonal spring allergies. Could there come a day when allergies are a thing of the past?

Remarkably, on that front, there is a glimmer of hope.

Scientists recently came a step closer to finally explaining why some allergies can last a lifetime while others fade. Turns out, the persistence of allergies may be linked to a unique type of immune cell — and someday, by modifying or deleting these cells, scientists could theoretically help make people's allergies less cumbersome or even cure them. 

Allergies have long puzzled scientists — researchers don't fully understand why allergies affect some people but not others, or why allergies emerge in the first place. Previous research has found that the type of antibody most often associated with allergies is produced by cells that don't last very long in the body, which makes people's lifelong allergies harder to explain. 

Two recent studies, published back-to-back in the journal Science Translational Medicine, might help solve that mystery. The studies, one of which examined children with allergies and the other adults, described a unique type of immune cell that hasn't been tied to allergies before.  

Related: Best air purifiers for allergies 2024 

The cells typically produce a type of antibody not associated with allergies, called immunoglobulin G (IgG). But a subset of these cells actually switch over to making an allergy-related antibody called immunoglobulin E (IgE) when confronted with an allergen, whether pollen, pet dander or peanuts.

IgE is usually produced by short-lived plasma cells, which churn out antibodies as an immediate and temporary line of defense for the body. These antibodies are thought to help fight off parasites, for instance, but in allergies, they go after harmless proteins instead.

The newly described cells are a type of memory B cell, which typically remember viruses and bacteria and spit out IgG when those invaders show up. But now, scientists have uncovered a subset of memory B cells that remember allergens and can make IgE. These cells are not short-lived like plasma cells and instead linger in the body for an indefinite amount of time — many years, or possibly a person's entire life.

The new research could be helpful in developing new treatments or tests for allergies — for instance, to assess if a childhood allergy is likely to persist into adulthood, the study researchers say. 

"These cells may be analyzed as sort of a [biological marker] for risk of allergy or allergy persistence," said Maria Curotto De Lafaille, a professor of pediatrics and of immunology and allergy at the Icahn School of Medicine at Mount Sinai Hospital in New York and senior author of the study on children.

That study focused on children with peanut allergies and analyzed blood samples from 58 kids who are allergic to peanuts and 13 who aren't. The second study analyzed a smaller number of blood samples from adults with a variety of allergies, including six with a birch-pollen allergy, four with a dust-mite allergy and 11 with peanut allergies.

While all the children with allergies avoided eating peanuts, participants in the adult study with birch-pollen allergies gave blood samples before and after starting an immunotherapy treatment for their allergies. This treatment is designed to desensitize the immune system by exposing patients to a small amount of allergen and then gradually increasing the dose over time. 

Both studies looked for signs that memory B cells might switch over to producing IgE after being exposed to allergens. For instance, researchers examining samples from children searched for B memory cells with a specific type of receptor, or part of the antibody that enables it to bind to specific proteins. This receptor is more common in people with eczema and asthma, two inflammatory conditions that often coincide with allergies, than in people without the conditions.

Related: Inflammation is a 'mismatch between our evolutionary history and modern environment,' says immunologist Ruslan Medzhitov

The two studies pinpointed the same type of memory B cell in people with allergies, although notably, earlier research had found similar cells in animals and in people with asthma and eczema. 

The cells "directly create IgE antibodies, the type that make us allergic," Joshua Koenig, an assistant professor of medicine at McMaster University in Canada and the first author of the paper focused on adults, told Live Science in an email. "They're really the long-term memory reservoir of allergy." 

The research is part of "an important area of study, and the key to understanding the persistence of diseases that are caused by antibodies, like allergies," Dr. Sarita Patil, an assistant professor of allergy and immunology at Harvard Medical School who was not involved in the studies, told Live Science in an email.

Both studies were limited by having a small number of participants. Future research could look at how immunotherapy for peanut allergies impacts the newly described cells and the antibodies that they release. It's known that the immunotherapy reduces people's allergen-specific IgE levels over time, but the impact on these memory B cells is unclear. 

Other future research could see whether the behavior of these cells changes over time, especially in children, who sometimes outgrow their allergies.

Understanding why allergies persist could one day help scientists eliminate or modify these allergy-specific cells so that they don't produce IgE and trigger an immune response anymore, Lafaille said. In other words, studies building on this research might one day help lessen the impact of allergies or even cure them.

Editor's note: This story was updated on April 12, 2024. It was first published on Feb. 16, 2024. 

This article is for informational purposes only and is not meant to offer medical advice.

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Women are up to four times more likely than men to be affected by autoimmune disease, conditions in which the immune system mistakenly attacks the body's own cells. Now, scientists think they know why: Women's outsized risk may be tied to how the body controls its X chromosomes. 

Humans have two types of sex chromosomes: X and Y. Most females carry two X chromosomes in each cell, while most males have an X and a Y. The X chromosome is larger than the Y and contains far more genes that code for proteins. But in people with two X chromosomes, only one needs to participate in protein production — otherwise, cells could soon be overwhelmed with too many proteins. To prevent this, one X chromosome in each cell is "silenced" in females during embryonic development. 

A long molecule of RNA — the genetic cousin of DNA — called Xist executes this silencing by latching onto one X chromosome. It turns out, however, that many proteins are prone to sticking to Xist, and these big complexes of RNA and proteins may predispose females to autoimmune disease. 

That's because the complexes can set off an immune reaction in which the body makes antibodies against the proteins within it, according to a new study in mice and humans published Thursday (Feb. 1) in the journal Cell. 

"So besides it's [Xist] job in controlling gene activity, there's really a major immunological imprint that maybe hadn't previously been recognized," Dr. Howard Chang, co-senior study author and a professor of cancer research and genetics at Stanford University, told Live Science. 

These findings could therefore open up new avenues for research into treatments for autoimmune diseases, he said.  

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower

Autoimmune diseases, which affect more than 23.5 million Americans, are caused by a combination of genetic and environmental triggers. Scientists have proposed many theories to explain why women are more likely to develop the conditions, pointing to their hormones and the microbes inside and on them, but none of these ideas have been conclusively confirmed.  

Earlier research by Chang and colleagues suggested that the Xist complex may drive sex-biased autoimmunity, as many proteins associated with autoimmune diseases could bind to it. But Xist needed to be studied in isolation, without other factors, such as hormones, that could potentially mask its influence. 

So the team genetically engineered two strains of male mice to make Xist: one that was genetically susceptible to autoimmune symptoms similar to those of lupus and another that was resistant — the comparison group. In the lupus-prone strain, female mice were more prone to symptoms than male mice were, so the team theorized that Xist would bring the males' levels of disease up to that of females. 

In their experiments, the team sewed a special version of the Xist gene into the genomes of male mice that could be switched on but wouldn't silence their only X chromosome. To stimulate autoimmune disease, they had to expose the lupus-prone mice to a specific chemical. 

Related: Inflammation is a 'mismatch between our evolutionary history and modern environment,' says immunologist Ruslan Medzhitov

Once Xist was activated and lupus was induced, the team saw that male mice that expressed Xist developed disease at a similar rate to females and had more severe disease than mice without Xist. 

However, requiring both the environmental chemical trigger and a genetic predisposition to lupus was an important control, Chang said. That made the mouse experiments more relevant to humans. 

"If someone is born with a genetic susceptibility, then the presence of Xist has some impact but also, very importantly, this environmental trigger [is necessary]," Chang said. Carrying Xist doesn't guarantee a person will have an autoimmune condition; the Xist complex may just account for the discrepancy in case counts between the sexes. 

To back up their mouse results, the team analyzed blood samples from more than 100 patients with autoimmune diseases, including lupus, and 20 without autoimmune disease. They discovered that the patients with autoimmunity had more Xist autoantibodies in their blood than the individuals without autoimmunity did. 

The types and numbers of autoantibodies in different people were disease-specific, which may help with the future diagnosis and treatment of these conditions, Chang said. For example, someday, taking these autoantibody profiles could help doctors decipher which disease a patient has or predict the trajectory of their condition, he said. 

This article is for informational purposes only and is not meant to offer medical advice.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

They're the hallmarks of cold and flu season: a sore throat, a blocked nose and, sometimes, a dreaded fever.

You may have heard that the warmth of a fever helps the body recover from illness. But how, exactly, do fevers help kill germs in the body?

Scientists know that elevated body temperatures play a role in helping the immune system fight infection: "The enhanced immune function during fever is at least partly caused directly by the fever because it can also be elicited by hyperthermia — that is, increased body temperature in the absence of an infection," Anders Blomqvist, a neuroscientist who studies fever at Linköping University in Sweden, told Live Science in an email.

But just cranking up the heat might not be enough to thwart an illness, so other immune factors must also be involved.

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower 

Fevers begin when immune cells at the site of an infection secrete pro-inflammatory cytokines — proteins that ramp up the immune response. To generate a fever, some cytokines travel to the brain and mess with the hypothalamus, which, among regulating other bodily functions, acts as the body's thermostat. There, the cytokines boost the production of enzymes that synthesize fever-triggering chemical signals called prostaglandins.

In fact, fever-suppressing drugs such as acetaminophen (Tylenol) and ibuprofen (Advil) are thought to work by blocking these enzymes from making prostaglandins. 

Prostaglandins initiate several changes in the body that trigger a fever, which is often defined as a body temperature of at least 100.4 degrees Fahrenheit (38 degrees Celsius). Acting through the chemical messengers of the nervous system, they boost heat generation within brown fat reserves, which burn sugar. They also induce muscle shivering to build heat, and they limit heat loss by constricting blood vessels, especially near the extremities, like the hands and feet.

But how does turning up the heat affect the scuffle between pathogens and the immune system?

"Febrile temperatures have been shown to increase the immune response by stimulating both the innate and adaptive compartments of the immune system," Blomqvist said. The former controls generalized immune reactions, while the latter "learns" to fight new pathogens as they enter the body. "But the underlying mechanisms are not fully understood," he noted.

However, there are specific elements of the immune system that fevers are thought to boost. First-responder immune cells called neutrophils are recruited to the front lines at an infected site; these cells die shortly after service, so fevers may encourage a larger number to be drafted to the battlefield.

There's also evidence that, during a fever, so-called dendritic cells develop a stronger tendency to engulf harmful microbes. By gobbling up germs, the cells can then present fragments of the microbes to adaptive immune cells, giving them intel on how to mount an attack tailored toward the invader.

Related: Can you catch a cold and the flu at the same time?

Researchers have also proposed that fevers might hamper a pathogen's chances of winning the battle by putting it in the hot seat. If a foreign invader evolves to infect the body at normal temperatures, its performance may dwindle when overheated as its enzymes might start to "cook," losing shape and functionality. But, if the pathogen evolves to withstand fevers, it might then become less adept at infecting people at normal body temperatures. In essence, the pathogen might find itself in a catch-22 scenario.

Scientists face a major challenge in figuring out how fevers fight infection: The cytokines that trigger fevers also enhance other immune functions, so it's difficult to tease apart the effect of the fever from these other immune boosts. For example, pro-inflammatory cytokines promote the migration of immune cells around the body. This ushers them to the infected site as well as immune tissues, like lymph nodes, where adaptive immune cells are trained to fight an infection.

Although the cytokines also play their part, Blomqvist argued that fevers play an important role in fighting foreign invaders. 

Studies show that intensive-care patients are more likely to recover from an infection if they develop a fever. The effect of fever-suppressing drugs is also telling: Doctors may feel it's necessary to administer them if they're worried a patient's fever will rise to dangerous temperatures, but in less severe cases, using these drugs might disarm the body's defenses.

"The most robust evidence for the beneficial effects of fever comes from preclinical and clinical studies showing increased mortality to infections when antipyretics [fever reducers] are given," Blomqvist noted. Critically ill patients were more likely to survive if they only received fever-reducing acetaminophen at the last minute, before their fever crossed the danger threshold.

This article is for informational purposes only and is not meant to offer medical advice.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

Most of the time, you probably barely notice the mucus in your nose. But when you have a cold or seasonal allergies, the glue-like goo that floods your nostrils suddenly makes breathing laborious and consumes your thoughts.

But have you ever wondered why snot is so remarkably sticky?

Mucus may be annoying when it's clogging your nose, but its stickiness serves an important purpose: It helps trap and remove tiny irritants that get sucked into your nasal passages along with inhaled air.

Without mucus, dirt particles and harmful microbes would reach lower parts of the respiratory tract and damage the delicate tissues in the lungs, Dr. Johannes Uys, a primary care physician at Broadgate General Practice, a clinic in London, told Live Science by email. Therefore, the consistency of nasal mucus plays an important role in your immune defenses, he said.

Related: What does it look like when your sinuses are clogged?

That said, snot is more than a physical barrier to airborne pollutants; it also contains antiviral and antibacterial components, including antibodies, proteins produced by the immune system to help prevent infections. Snot also contains lysosomes, specialized cell units containing enzymes that break down invading pathogens, according to the medical resource StatPearls.

The consistency of your snot can tell you a lot about your health, when you couple that information with other symptoms, Dr. Jay Lee, a member of the board of directors of the American Academy of Family Physicians, told Live Science by email.

"While normal mucus is clear and watery, cloudy or discolored mucus ― like green or yellow ― could signal that you have a viral or bacterial infection," he said. That's because snot contains dead white blood cells, a type of immune cell, and other waste products left over from an immune response. So during an infection, it changes color.

"You may also notice a lot of congestion, because infections can lead to inflammation in the [mucous] membranes that line the nasal airway, causing airway glands to produce more mucus," Lee said. The mucus not only increases in volume, but it also gets thicker ― again, that is due to an accumulation of dead microbes and cells that arrived to fight the infection.

To a large extent, snot owes its stickiness and gel-forming properties to molecules known as mucins, Lee said.

The structure of these sticky molecules resembles bottlebrushes: They have a thin, elongated protein backbone with thick, bristly carbohydrate branches sticking out of it. This unique shape allows mucins to bind with each other in a network that can resist changing shape. For this reason, mucus in your nose can rapidly snap back to its initial shape even if its structure is briefly disrupted when you cough or blow your nose, according to a 2018 review published in the journal Annual Review of Cell and Developmental Biology.

The chemical structure of mucins also gives them the ability to bind significant amounts of water, which is what contributes to the thick, gelatinous texture of snot, Uys noted.

Mucins are a scaffolding for other active components in the mucus, but they do much more than that. For example, these sticky molecules can interact with the microbes that naturally reside inside the mucous barrier, serving as a source of fuel. While supporting the growth of some bacteria, mucins can also help prevent harmful microbes, such as the bacterium Staphylococcus aureus or the yeast Candida albicans, from adhering to the walls of your nose, the Annual Review authors noted.

So, next time you're struck with a stuffy nose, remember the silver lining: Your snot is helping you fight off the infection.

This article is for informational purposes only and is not meant to offer medical advice.

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Any parent of young children dreads hearing the words "pink eye." This common childhood infection, also called conjunctivitis, can spread rapidly, and once the little ones bring it home, it can be passed easily to other members of the household. 

But why is pink eye so contagious?

One factor is that conjunctivitis, or inflammation of the conjunctiva — a thin, clear mucous layer that covers the inner surface of the eyelid and the white part of the eyeball — is often caused by very infectious bacteria and viruses, Dr. Paramdeep Bilkhu, an optometrist and clinical adviser at the College of Optometrists in London, told Live Science by email. 

Although allergies or irritants such as a loose eyelash can cause pink eye, most cases come from viruses and bacteria. Adenoviruses, a highly contagious family of pathogens that also cause cold- and flu-like symptoms, account for over 75% of cases of infective conjunctivitis, Bilkhu said. 

Adenoviruses are also extremely hardy. For example, these viruses may survive disinfectants, such as 70% rubbing-alcohol (such as common hand sanitizers) and 3% hydrogen peroxide (such as Lysol and other household cleaners) solutions, according to a 2020 systematic review published in the Journal of Ophthalmic & Vision Research.

What's more, a person infected with an adenovirus can be contagious for up to two weeks from the time they are infected. Lastly, no treatments target adenoviruses, the review authors noted.

"While in some cases of bacterial infective conjunctivitis antibiotics are required to help bring about resolution, they will not work where the cause is viral," Bilkhu said. "There are no antiviral agents available to treat the viruses typically implicated in infective conjunctivitis."

Related: What are eyes made of?

The bacteria and viruses behind pink eye spread as a direct result of the symptoms they cause, such as red, watery eyes; sticky discharge; and a burning or itching sensation. People with pink eye have an intense urge to rub the affected eyes. From those infected surfaces, the microbes can go from someone's hands to surfaces and personal items, according to the Centers for Disease Control and Prevention (CDC). 

Viruses that cause pink eye also may be transmitted through droplets expelled when someone coughs or sneezes. That is because they are able to spread along the mucous membranes that connect the respiratory tract, tear ducts and conjunctiva, according to the American Optometric Association. "Many cases of viral conjunctivitis occur following a prior or close contact with someone who has an upper respiratory tract infection, such as a cold or flu," Bilkhu said. 

Because young children spend a lot of time in close contact with each other and do not tend to practice good hygiene, they are particularly susceptible to pink eye, according to the American Academy of Ophthalmology. 

Most cases of infective conjunctivitis are mild and resolve within two weeks without any long-term complications. "During this period, the key is to ensure careful hygiene measures to prevent spread to the fellow eye and to others," Bilkhu said. "This includes washing hands before and after touching the eyes, appropriately disinfecting surfaces after touching them, and changing bedding and pillow cases each night."

This article is for informational purposes only and is not meant to offer medical advice. 

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website! 

Basking in the sun can cause a number of health conditions, from sunburn to skin cancer. But can you be allergic to the sun, too?

The short answer is, yes, you can have an allergic reaction to ultraviolet light from the sun. A sun allergy produces an itchy rash that may present as red bumps, red patches, blisters or hives on the sun-exposed areas of the skin, Dr. Debra Jaliman, a board-certified dermatologist based in New York and a member of the American Academy of Dermatology, told Live Science.

However, the term "sun allergy" is an umbrella term that encompasses several immune responses to ultraviolet light. Some sun allergies may be linked to a person's genetic make-up, while others can develop in response to certain chemicals from medicines or cosmetics, according to Harvard Health.

Related: What causes allergies?

Polymorphic light eruption (PMLE) is one of the most common forms of sun allergy. PMLE may affect 1 in 10 people worldwide, but it tends to be more prevalent in the Northern Hemisphere, according to a 2022 meta-analysis published in the Journal of the European Academy of Dermatology & Venereology. PMLE usually manifests as a rash that appears within two hours of sun exposure. This condition typically affects more women than men, and its symptoms often begin in early adulthood. Scientists don't know what causes PMLE, according to the medical resource StatPearls.

In rare cases, PMLE may be hereditary. This form of sun allergy, called Actinic prurigo, predominantly affects Native American populations in the northern, southern and central U.S. The symptoms of Actinic prurigo often begin earlier — and are more severe — than in typical PMLE, Harvard Health noted.

Another common form of sun allergy is photoallergic eruption, a skin reaction triggered by an interaction between sunlight and chemicals either ingested or applied to the skin. This blistery rash may take one to two days to develop and can spread to areas of the skin that were not exposed to the sun, according to Harvard Health. Photoallergic eruption "can occur in people of all skin types, but light-skinned individuals who are more sensitive to the sun are more likely to get the symptoms," Jaliman said.

Photoallergic eruption is often caused by synthetic chemicals found in topical cosmetics, including musk fragrances and benzophenones, an ingredient in some mineral sunscreens. But natural substances, such as lime juice, can trigger it too, she said. A number of prescription medications, including "certain antibiotics, such as tetracycline and ciprofloxacin; sulfur-based drugs, like hydrochlorothiazide [a diuretic]; and isotretinoin, a medication used to treat acne," can also cause photoallergic eruption, Jaliman noted.

Solar urticaria is another form of sun allergy, although most doctors consider this condition rare, according to Harvard Health. People with solar urticaria tend to develop hives and bumps on the skin immediately after being exposed to sunlight. It is not known what causes this condition, according to StatPearls.

Jaliman emphasized that anyone can develop a sun allergy, even if they have never had an adverse reaction to ultraviolet radiation. "For example, you could take a certain antibiotic for years, but then one day develop a photoallergic reaction to it," she said. "Unfortunately, [these] allergic reactions can develop over time."

This article is for informational purposes only and is not meant to offer medical advice.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website! 

"Inflammation is the new evil. Let me explain."

"You might think inflammation isn't really THAT big of a deal…but trust me when I say it is." 

Scan social media and you'll easily find content that portrays inflammation as a villain. 

In every bookstore you'll find at least one anti-inflammatory diet recipe book, and in your local drug store, an array of products parading their magical anti-inflammatory ingredients. 

But inflammation has evolved over millennia to protect us, says Ruslan Medzhitov, a Sterling Professor of Immunobiology at Yale University School of Medicine and Investigator at the Howard Hughes Medical Institute in Maryland who studies inflammation in the context of autoimmune disease and allergies. 

Related: 'If you don't have inflammation, then you'll die': How scientists are reprogramming the body's natural superpower

So if not all inflammation is bad for us, how do we know the difference between "good" and "bad?" 

Live Science spoke with Medzhitov about how inflammation is the body's response to a system out of equilibrium, how chronic inflammation results from a mismatch between our evolutionary environment and the modern one, and whether there's any evidence for specific "anti-inflammatory" diets.

Emily Cooke: What is inflammation?

Ruslan Medzhitov: Inflammation is an essential part of our defense system. It evolved to protect us from a variety of challenges, including many challenges that come from the outside world, such as infection or injury or toxins. Without inflammation, we would quickly succumb to infections and die and that would be the end of it. 

Mostly what we know about inflammation is what happens at the extreme, when there is an infection or injury and then there is swelling and redness and fever and things like that. But inflammation plays an important role in a variety of settings, including when we don't diagnose it clinically as inflammation, including when we may not even feel it, it's asymptomatic. 

Under the hood, it plays an important role in coordinating metabolism, different physiological functions and so forth. Those functions of inflammation are much, much less appreciated and much less studied. And just to give one quick example of the reach of inflammation throughout biology is that it controls our metabolism, controls adaptation to the environment in terms of thermogenesis [heat production] and [even controls] aspects of behavior. And that last part is what's particularly interesting, where inflammation can for example, control mood. It can control avoidance behaviors, and anxiety behaviors. And these are all presumably by design, meaning that these are meant to be protective phenomena, they're beneficial in certain settings. When this response becomes dysregulated in some way, it can lead to particular types of pathologies and disorders and so forth that inflammation unfortunately is more famous for. 

Related: Brain inflammation may drive mood changes in Alzheimer's

EC: Is there such a thing as "good" and "bad" inflammation?

RM: Yes, and there are two ways to divide between good and bad inflammation. 

So, good inflammation operates within the normal range. What is "normal" is decided not by us, by how we feel. It is decided by millions of years of evolution and calibrated by, on average, if you have this type of response, on average you have a better chance for survival. But that was in a very, very different setting. Throughout our evolutionary history, of course, our environment was very different. But the genes that evolved under those conditions, we still have them and they still operate as if nothing [has changed], because dramatic change in the environment happened only very recently. 

Good inflammation will be the one that operates with the right magnitude, that provides maximum benefit and lowest possible cost. 

But that line is very fuzzy and one can shift into what would be now called "bad" inflammation, which is a protective response but in overdrive. 

Phenomena like cytokine storms [when chemical signals associated with inflammation go haywire], sepsis [an over-reaction to infection], anaphylactic shock [a severe allergic reaction], these are all examples of inflammation that went way too far in magnitude, so it's induced too strongly. 

Again, what is a good magnitude versus too much? The logic of it is decided by evolution. 

So one delineation of good inflammation [versus] bad inflammation is just the magnitude of the response. 

The second type is when inflammation may be induced in the right magnitude, but it's induced for the wrong reasons. And that is what often leads to chronic inflammation. But the reason that happens is, again, in large part, a mismatch between our evolutionary history and modern environment. [Being obese was uncommon in our evolutionary past], because that would be unheard of under normal, natural conditions where you have to walk for 10 miles to find something to eat every day. 

In the modern environment, obesity is common. But that's not what our genes evolved to deal with and they misinterpret it, induce inflammation and then obesity-associated inflammation then becomes a problem. 

And the second example of that is aging-associated inflammation. Most of our ancestors throughout history would be dead by 30 years of age. Therefore the body is not, sort of, designed to deal with changes that happen at an advanced age. Many age-related deteriorations in body functions can be interpreted by inflammation as, "oh, something is off, I'm supposed to get in action when something gets off a normal homeostatic [self-regulating] range." And what happens then? It creates this vicious cycle where, [in response to] these deviations that are age-related or obesity-related or [related to] other evolutionarily-new and modern aspects of our lifestyle, inflammation is induced. [The body is] thinking "I will try to fix it." But there's nothing to fix. And that's what is, really, mostly bad inflammation. 

Related: DNA-damaging gut bacteria may fuel colon cancer in patients with inflammatory bowel disease

EC: Is it possible to modulate "bad" inflammation with lifestyle changes, for example with anti-inflammatory diets? Is the evidence actually there? 

RM: Yes, it is possible to modulate it.  But if you look at the common denominator —  so exercise, diet, healthy food, diverse food, avoid processed foods, avoid sedentary lifestyle, have enough sleep, reduce stress — if you think about what is the common denominator, all of them have one thing in common: modify your lifestyle to approximate, slightly better, the way we evolved to be. 

EC: From an immunobiology perspective, what message would you want people to know if they were concerned about inflammation? 

RM: Well, I would say that inflammation in general is something that we all need to protect ourselves. We don't want to completely eliminate it, that would be lethal basically. Without inflammation we cannot survive. That most causes of unwanted or "bad" inflammation in the modern world, in industrialized countries at least, have to do with aspects of our lifestyles that are unnatural and unhealthy. And I think diet and physical activity are probably the major drivers. 

I mean, this is not anything new. 

But having said that, there are also conditions that are truly pathological, like autoimmune diseases, for example, or sepsis, and that's where inflammation is mostly evil and mostly just needs to be knocked down and controlled. 

But for the majority of people this has to do with chronic inflammation that may be even asymptomatic, sub-clinical, but under the hood slowly contributes to various sorts of unhealthy conditions. And that's where the steps of simple interventions of having the right diet and the right physical activity [come in.]

And I would just add one more thing. Nobody knows what the right diet actually is. I think it's a failure, both on the part of the scientists, and the part of communicators of science. Because if the science is not there, what do you communicate? 

And that's that we don't really understand food. We don't understand what a healthy diet is. We don't understand how it affects our bodies. We know some obvious things, trivial things, calories and things like that, vitamins. But beyond that our knowledge is really at the medieval level. 

And that, I think, is going to be the next big frontier in biomedical science. So when I say healthy food, healthy diet, I'm just saying it in sort of, in terms of the obvious aspects of it. Eating processed food, highly processed simple sugars, high calorie, unbalanced, those are things that are obviously bad. But beyond those trivial aspects, there is a lot more to it that we don't really understand. So, I say healthy diet, but with the qualification that we only know very little about what a healthy diet really is. 

Editor's Note: This interview has been condensed and edited for clarity.

Inflammation is one of the body's superpowers. It helps us fight off infections and heal wounds.

"If you don't have inflammation, then you'll die," Ed Rainger, a professor who studies chronic inflammation at the University of Birmingham in the U.K., told Live Science. "It's as simple as that."

But if it transitions from a short-term response to one that lingers for months or years, chronic inflammation can fuel diseases such as cirrhosis, rheumatoid arthritis (RA) and heart disease.

In the past, doctors tried to treat these diseases by shutting down all inflammation, which has nasty side effects and doesn't always work. But now, scientists are designing treatments that don't eliminate inflammation altogether but rather reprogram the cells that fuel it.

And in diseases like cancer, where tumors hijack the healing side of inflammation to fuel their growth, new treatments are instead taking the opposite approach — pushing inflammation back into a fighting state so that it can better attack these mutated cells.

Depending on the context, inflammation can be seen as helpful or harmful, but thanks to new research, in either case, it can be brought back under control.

"If you can do that, then you can let the immune system and the inflammatory response get on with it, just in a normal way," Rainger said.

Related: Inflammation is a 'mismatch between our evolutionary history and modern environment,' says immunologist Ruslan Medzhitov

Acute and chronic inflammation

Inflammation is the body's natural response to physical trauma, infection or toxins, and doctors have been describing it since antiquity. "Inflammare" means "to set on fire" in Latin, and in the second century, Galen, the physician of Roman emperor Marcus Aurelius, described its five "cardinal signs" as heat, redness, swelling, pain and loss of function.

What these early doctors were describing were the hallmarks of acute inflammation. The redness and heat are caused by the local dilation of blood vessels to ferry more cells to the damaged tissue, while the release of compounds such as prostaglandins cause pain and swelling. To thwart infections, the immune system also cranks out chemicals called pyrogens that further crank up prostaglandin production, causing fever.

"The whole point of inflammation is to control an infection, stop it spreading and then allow the healing process to start," Robert Anthony, an associate professor of medicine at Harvard University, told Live Science.

During acute inflammation, damaged cells send out "danger" signals that lure immune cells to the site of the attack. These first responders include the amoeba-like macrophages that gobble up harmful invaders and neutrophils, which trap and kill these enemies. Once activated, these cells produce chemicals called cytokines, which amplify inflammation in a positive feedback loop.

As this acute inflammation rages, the immune system is learning to target the enemy more selectively.

Normally, acute inflammation peaks around seven days after the initial attack and starts to resolve around three days later, Anthony said. At the same time, certain cells work to heal wounds, secreting anti-inflammatory signals and promoting the formation of new blood vessels and connective tissue.

Scientists don't fully understand how the body switches off acute inflammation. But sometimes — for instance, if the immune system can't fully control an infection — it doesn't. Then, inflammation can morph from essential to harmful.

If "you stop that transition about day 10, that's when things transition into the chronic phase," Anthony said.

In chronic inflammation, neutrophils, macrophages and other white blood cells linger at the site of inflammation. They churn out cytokines, which keep inflammation amped up. Inflammatory cells also produce growth factors that fuel cell division and enzymes that cause tissue damage, which then sends out more "danger" signals to keep the loop going.

Chronic inflammation is implicated in a range of diseases, including RA, which affects the joints; cirrhosis, or severe liver scarring; and atherosclerosis, or plaques in blood vessels that can lead to heart attack and stroke. And the cellular proliferation and mutation induced by chronic inflammation can create a perfect environment for cancer to develop.

Related: Brain inflammation may drive mood changes in Alzheimer's

Historical treatment

In the past, treatments aimed to silence inflammation altogether. For instance, in the 1950s, scientists discovered the anti-inflammatory effects of a group of naturally occurring compounds called steroids, which turn down the volume on the broader immune response. Since then, steroids have become a mainstay treatment in chronic inflammatory diseases such as RA. But in addition to broadly suppressing the immune system, steroids can cause side effects such as high blood pressure, stomach ulcers and mood swings.

Then, in the 1990s, pharmaceutical companies began rolling out drugs called biologics. Many of these work by silencing different cytokines, the chemical signals that amplify inflammation.

However, like steroids, biologics often suppress large swaths of the immune system, which can increase the risk of infection. For instance, the drug tofacitinib, for RA, targets a signaling pathway which is shared by many cytokines and as a result can make people more vulnerable to herpes zoster virus, pneumonia and urinary tract infections. And for reasons we don't fully understand, biologics don't work for every patient.

So scientists are searching for more targeted ways to redirect harmful inflammation, often by reprogramming immune cells involved in the process.

Related: Why do coughs linger after a cold?

Cellular reprogramming

Stuart Forbes, director of the Centre for Regenerative Medicine and the Institute for Regeneration and Repair at the University of Edinburgh in the U.K., has been studying the role of macrophages in scar tissue formation in liver fibrosis. He and others have found there are actually two types of macrophages: a damaging inflammatory type, dubbed M1, and a second type, called M2. His research in mice found that this second type turned off inflammation and fueled tissue regeneration.

So Forbes' team filters macrophage precursor cells called monocytes from the blood of patients with severe liver scarring. In a lab dish, the team uses chemical signals to nudge these monocytes to become the regenerative, M2 version. Researchers then infuse these reprogrammed macrophages back into patients.

"Using our approach, what we're trying to do is stimulate regeneration of these livers, which means breaking down scar tissue and it means changing the inflammation from damage-forming inflammation to repair-forming inflammation," Forbes told Live Science.

The approach was found to be safe in a Phase I clinical trial of nine patients in 2019, with "encouraging" results from a Phase II efficacy trial in 50 patients presented by Forbes in November at a meeting of the American Association for the Study of Liver Diseases, he said. The team found that over the year-long trial, macrophage treatment decreased the number of potentially fatal, liver-related complications, compared with a control group that did not receive the treatment.

Related: Teen's year-long case of depression and seizures caused by brain-injuring autoimmune disease

Tissue-specific cells

However, to treat the root problem in inflammatory diseases, you need to know the critical cells in specific tissue, Dr. Chris Buckley, a professor of translational rheumatology at the University of Oxford, told Live Science.

For instance, in RA, white blood cells that are part of the adaptive immune system mistakenly target joint tissue. These white blood cells activate macrophages and connective-tissue-forming cells called fibroblasts, which fuel joint inflammation. Typical RA treatments target the rogue white blood cells. Yet only 50% of patients with RA enter remission.

But in a 2019 paper in the journal Nature, Buckley and colleagues discovered that one type of fibroblast in the joint drives inflammation in RA, while another drives bone and cartilage damage in osteoarthritis. This raises the prospect of treating these diseases by targeting the fibroblasts unique to each condition: inflammatory fibroblasts in RA, and the bone- and cartilage-damaging ones in osteoarthritis.

For RA, for example, if they could target both the white blood cells and the fibroblasts, they might get 100% remission, Buckley said.

The treatment is in its early phases. However, in 2021, a drug called seliciclib, which suppresses the proliferation of fibroblasts in the joints, was found to be safe in a Phase I clinical trial in 15 patients with RA, clearing the path for future trials to assess the drug's efficacy.

Related: DNA-damaging gut bacteria may fuel colon cancer in patients with inflammatory bowel disease

Fanning the flames for good 

In some chronic diseases, scientists are developing therapies that stimulate inflammation.

In cancer, for example, macrophages migrate to tumors and attack them, but cancer cells hijack this process, releasing chemicals that cause macrophages to switch from the pro-inflammatory M1 type, to the regenerative M2 type, which suppress inflammation and promotes tumor growth.

Armed with this knowledge, Dr. Yara Abdou, an assistant professor of oncology at the University of North Carolina and her colleagues wondered whether they could use a virus to make macrophages in cancer patients more likely to recognize and attack tumor cells, essentially acting like M1 macrophages.

In 2022, early results from an ongoing Phase I clinical trial of 18 patients with different types of solid cancer — including breast, ovarian and esophageal cancer — showed that treatment with these re-programmed macrophages, called CT-0508, was safe and had promising results.

"We were also able to see that CT-0508 is capable of inflaming the tumor microenvironment," Abdou told Live Science in an email. These macrophages also recruited and activated other immune cells tasked with destroying cancer, she said.

More data from the trial will be reported in 2024, Abdou said. Based on these "encouraging" results, the team also plans to test an alternative version of this therapy called CT-0525, which uses reprogrammed monocytes instead of macrophages, in a Phase I clinical trial in 2024.

Related: What happens to cancer cells after they're killed by treatments?

Next steps

With a Phase II clinical trial under their belt, Forbes and his colleagues want to test an advanced version of their macrophage therapy in patients who have been hospitalized with cirrhosis.

"Currently liver transplant with lifelong care is the only option for patients with advanced liver cirrhosis," Forbes said. Macrophage therapy could therefore provide "a new therapeutic option for this large and growing patient population."

At the cellular level, Buckley would like to learn more about what drives fibroblasts to both the inflammatory and cartilage-damaging state, teasing out whether the two forms develop from a common precursor cell and determining what factors may regulate this process.

Knowing more about these fibroblasts, both in health and disease, could "unlock their therapeutic potential in tissue repair," Buckley and his colleagues wrote in a 2021 review article.

As for the cancer therapy that is being developed by Abdou and her team, many questions remain, she said. For instance, the team needs to fine tune the exact dose that would be given to patients and assess which type of cancer it may be more effective against.

They're hopeful though that they'll be able to move on to the next stage of testing, a Phase II clinical trial, and if successful, one day, roll it out in patients.

Ultimately, what Abdou and others are doing is reframing the way that we see inflammation; not solely as a flaw to be fixed, but rather an incredible force that can be controlled and harnessed for good.

Rare blood clots tied to some early COVID-19 vaccines that are no longer in use may have been the result of two out-of-control immune reactions happening at once.

One of these immune reactions was already known, but the second, reported Oct. 26 in the journal Blood, is a new discovery.

The finding could help to explain how other clotting conditions develop and point to better treatments, as well as suggest ways to make vaccines safer for people who are prone to the side effect.

"Understanding how a drug causes an adverse event allows us to design new approaches to make those treatments safer," said Ishac Nazy, an associate professor of medicine at McMaster University in Canada who studies the vaccine-related clotting disorder but was not involved in the current research.

A rare side effect

The vaccine-related clotting disorder, known as vaccine-induced immune thrombotic thrombocytopenia (VITT), was rare and linked to two shots: the Johnson & Johnson (J&J) and AstraZeneca COVID-19 vaccines. Both shots contained common-cold viruses called adenoviruses that were tweaked so that they couldn't infect cells. Instead, the modified viruses carried DNA instructions for part of SARS-CoV-2, the coronavirus that causes COVID-19, into the body.

VITT was a sobering side effect of what many public health experts had hoped would be a promising technology. Unlike the Moderna and Pfizer-BioNTech COVID-19 shots, which contain RNA, the J&J and AstraZeneca vaccines did not need ultracold storage, making them more accessible where cold-chain storage is unreliable. Adenovirus-based vaccines have been investigated for other diseases, but very few have achieved approval. Exceptions are an adenovirus-based Ebola vaccine approved in China and another approved by the European Union, both used only in at-risk individuals.

Soon after rolling out the J&J and AstraZeneca vaccines, doctors began reporting cases of clotting that looked a lot like a previously known disorder called Heparin-induced thrombocytopenia (HIT). About 20 to 30 years ago, HIT affected 3.5% of patients who had knee or hip replacements, said Dr. Andreas Greinacher, a physician who specializes in clotting disorders at the Greifswald University Hospital in Germany and was not involved in the new research. In these patients, heparin, a blood thinner normally given to prevent blood clots, actually triggered runaway clotting instead.

The adenovirus-based COVID vaccines were triggering the same condition as HIT, though scientists gave it a new acronym to reflect the different origin. Researchers reported that about 1 in 50,000 people under 50 who received the vaccine were affected, as well as about 1 in 100,000 of those 50 and older.

Neither vaccine is currently administered in the U.S. (AstraZeneca's shot was never used in the country, and J&J's vaccine was authorized but then retired due to the clotting issue and availability of better vaccines.) However, learning what triggers VITT could still be useful.

Today, HIT is rare because doctors now understand what causes it and can prescribe different, safer versions of heparin, Greinacher told Live Science. Similarly, he said, studying the mechanisms behind HIT and VITT could make adenovirus vaccines safer.

"Our big aim currently is to find which factor in the vaccines is triggering it," Greinacher said. "If you know the factor, I'm certain there are very smart biotechnologists who can modify the adenovirus vector so this factor is no longer present."

Unraveling VITT

When VITT was first observed in patients getting COVID-19 vaccines in February 2021, scientists soon discovered that it had to do with PF4, a chemical signal released by platelets, the blood cells that form clots.

In rare cases after vaccination with an adenovirus-based vaccine, the body would make antibodies to PF4. These antibodies would latch onto PF4 and form clumps that could then bind to receptors called Fc on other platelets. This would activate the platelets and lead to a runaway clotting response.

The new Blood study found that PF4 alone also activates a second set of receptors that cause platelets to accumulate, likely a second reason why clotting goes haywire in this disorder.

There is still a long way to go, Nazy told Live Science, whose team first reported in 2021 how antibodies against PF4 were causing VITT. The new research suggests that there are actually two different ways that PF4 acts in VITT, he said. These two pathways are not exclusive and may work in tandem.

In the new study, researchers tested blood from healthy individuals and people with VITT to trace the cascade of signals that leads to the overactive clotting. They found that the PF4 activates a receptor called c-Mpl on platelets, which causes them to clump together. This is in addition to the mechanism discovered in 2021, in which complexes of PF4 and PF4 antibodies activate platelets' Fc receptors.

"What we have shown is that as well as that antibody trigger, you've also got PF4 itself binding to platelets and activating them, providing a double whammy," Phillip Nicolson, an associate clinical professor of cardiovascular medicine at the University of Birmingham in the U.K. and the leader of the new study, told Live Science. "That may be why [the clotting] happens to a harmful degree."

Scientists have a few clues as to why adenovirus vaccines can trigger this response. PF4 carries a positive electrical charge on its surface, while adenoviruses are highly negatively charged, Nicolson said, so they may bind together easily. But even that is not confirmed, Nazy said, and has mostly been shown with computer modeling rather than with real molecules.

In rare cases, unusual clotting happens without vaccination or treatment with heparin. A recent paper published in the The New England Journal of Medicine, and co-authored by Nazy, found that in at least two of these unexplained clotting cases, the clotting disorder occurred after typical adenovirus infections. In many cases, the connection between unexplained clotting and a viral infection may be missed. And it's still a mystery why very few people are susceptible to these clotting conditions.

"That's the part we need to understand to prevent the disease from even happening," Nazy said.

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website! 

Hospitalization is supposed to make people well. But on a given day, an estimated 1 in 31 hospitalized patients contracts an infection from the hospital itself, and tens of thousands die annually. Many of these infections are antibiotic-resistant, and treating them contributes to the evolution of new "superbugs."

But now, researchers have a new idea for preventing hospital-acquired infections: a vaccine that puts the immune system on short-term high alert for a broad array of pathogens.

The vaccine, so far tested only in mice, activates the innate immune system, the body's first line of defense, according to a study published Oct. 4 in the journal Science Translational Medicine. The innate immune system is not specific to any particular pathogen, and its protection tends to fade faster than that of the adaptive immune system, which "remembers" viruses and bacteria it has encountered in the past. (Most vaccines train the adaptive immune system to fight off specific diseases, such as the seasonal flu or COVID-19.)

But for hospitalized patients, broad and short-term protection is needed most, said Brad Spellberg, the senior study author and chief medical officer at the Los Angeles General Medical Center.

"It solves a problem that traditional vaccines have not been able to solve," Spellberg told Live Science.

Related: Dangerous 'superbugs' are a growing threat, and antibiotics can't stop their rise. What can?

There are too many potential hospital-acquired pathogens to reasonably vaccinate incoming patients for each individual bacterium or fungus, Spellberg said. And in any case, traditional vaccines require time to activate adaptive immunity, and hospitalized patients need immediate protection.

The researchers stumbled across the idea for the new vaccine more than 15 years ago while looking to develop a traditional vaccine for Staphylococcus aureus, a common source of hospital infections. Certain strains of the bacterium, known as methicillin-resistant S. aureus (MRSA), are resistant to common antibiotic treatments. 

The researchers were struggling to find a combination of bacterial proteins that would protect against staph infections in the blood, so they began adding a series of compounds called adjuvants to their formulation. Adjuvants are ingredients that broadly boost the immune response to a desired target.

Eventually, the researchers found a combination of three bacterial proteins and three adjuvants that worked in animal studies. But during testing, they found that giving mice a vaccine with only the three adjuvants was just as protective as giving them the vaccine with proteins and adjuvants combined.

"We were like, 'Whoa, whoa, whoa, what is going on here?'" Spellberg said.

What was going on, another decade of testing revealed, was that the vaccine was not specifically targeting the staph proteins. Rather, it was boosting the activity of the innate immune system more broadly — and that was enough to protect the mice from staph infection.

"It's an important and exciting concept for a vaccine," said Marcela Henao Tamayo, an immunologist at Colorado State University who was not involved in the new study.

The three adjuvants — aluminum hydroxide, monophosphoryl lipid A, and fungal mannan — protected mice against not only S. aureus but also strains of other common hospital-acquired pathogens with various degrees of antibiotic resistance, such as Enterococcus faecalis, Escherichia coli, Acinetobacter baumannii and Klebsiella pneumoniae. The vaccine also protected against the fungi Rhizopus delemar and Candida albicans, which also frequently affect hospitalized people.

Related: Cleaning product residues may be driving a deadly superbug's antibiotic resistance

Aluminum hydroxide and monophosphoryl lipid A are already used in vaccines and approved by regulatory agencies in both the U.S. and Europe, Spellberg said. Mannan, a component of fungal cell walls, is not yet an approved vaccine adjuvant, but it has been tested in humans in other medications without apparent safety issues, he said.

The research also found that the key reason the adjuvant-only vaccine worked was that it activated macrophages, immune cells that engulf and destroy foreign invaders. The researchers also observed other changes in the immune system, such as an increase in anti-inflammatory immune proteins called cytokines, and a decrease in pro-inflammatory cytokines. Though all the mechanisms aren't clear, this ratio has been linked to better survival after infection in previous studies, the researchers wrote. 

In mice, the vaccine's protection persisted for 28 days.

Giving this vaccine to patients upon hospitalization or before outpatient surgery could reduce the rate of hospital-borne infections and help combat the problem of antibiotic resistance, study co-author Jun Yan, a doctoral student in microbiology at the University of Southern California.

"By reducing the infection rate in the hospital, we're also reducing the new emergence of antibiotic resistance, because we can also reduce the use of antibiotics in hospitals," Yan told Live Science.

Human testing is the next step. Other vaccines, such as the live tuberculosis vaccine, have long been known to trigger an innate immune response in addition to raising the body's guard against specific germs, Henao Tamayo, who studies those vaccines, told Live Science. But getting a nonspecific vaccine approved by the Food and Drug Administration (FDA) is new territory, Spellberg said. The research team is currently in talks with the FDA about what kind of testing would be needed, and they hope to begin clinical trials in 12 to 18 months.

"I think what they have already developed is highly promising," Henao Tamayo said, "and we could learn a lot from human studies."

For immune health, some influencers seem to think the Goldilocks philosophy of "just right" is overrated. Why settle for less immunity when you can have more? Many social media posts push supplements and other life hacks that "boost your immune system" to keep you healthy and fend off illness.

However, these claims are not based on science and what is known about immune function. Healthy immune systems don't need to be "boosted." Instead, the immune system works best when it is perfectly balanced. Scientific experts on the immune system — immunologists — know that too much of an immune reaction could result in allergies, autoimmune disorders or chronic inflammation. On the flip side, too little of an immune reaction could result in illness or infection.

Your immune system requires a delicate balance to operate properly. When it's out of balance, your immune system itself can cause disease.

Related: New 'inverse vaccine' could wipe out autoimmune diseases, but more research is needed

Cellular balance

The immune system is the mobile defense system of your body. It is a complex network of cells and organs that work together to protect your body from infection and disease. Your immune cells are continually on patrol, traveling throughout your body looking for infectious invaders and damage.

New immune cells are created in your bone marrow. Certain immune cells — called B and T cells — are the special forces of the immune system, playing an important role in the elimination of infectious invaders. Because of this role, these cells undergo a rigorous boot camp during their development to ensure they will not discharge friendly fire on healthy cells in the body.

Any B cell or T cell exhibiting activity against the self — or autoreactivity — is killed during training. Millions of newly created B and T cells are killed every day because they fail this training process. If these self-reactive cells escape destruction, they could turn against the body and carry out an inappropriate autoimmune attack.

My research investigates how B cells are able to slip past the checkpoints the immune system has in place to guard against autoreactivity. These tolerance checkpoints ensure that autoreactive immune cells are either purged from the body or held in permanent lockdown and unable to engage in inappropriate responses that would target healthy tissue.

More isn't necessarily better

You've likely seen advertisements for dietary supplements that promise to "boost immune function." While this may sound appealing, it is important to keep in mind that the immune system functions best when perfectly balanced.

If the immune system is like a thermostat, turning it up too high results in overactivation and uncontrolled inflammation, while turning it down too low results in a failure to respond to infection and disease.

Because sustaining immune balance is critical, tinkering with the immune system through the use of supplements is not a good idea unless you have a clinical deficiency in certain vital nutrients. For people with healthy levels of nutrients, taking supplements could lead to a false sense of security, particularly since the fine print on the back of supplements usually has this disclaimer about their listed benefits: "This statement has not been evaluated by the FDA. Not intended to diagnose, treat, cure, or prevent any disease."

Eating a well-balanced diet, exercising regularly, reducing stress and getting decent sleep, on the other hand, can help your body maintain a functioning and healthy immune system. Although these lifestyle behaviors are not foolproof, they contribute to overall good health and ultimately to a more healthy immune system.

In reality, vaccines are the only safe and effective tool beyond healthy lifestyle behaviors to support your immune system. Vaccines contain harmless forms of pathogens that help to train your immune cells to recognize and fight them. When you come into contact with the real and harmful version of the pathogen out in the wild — whether it's at a grocery store, social event or school — at a later date, these fully trained immune memory cells will immediately begin to fight and destroy the pathogen, sometimes so quickly that you don't even realize you've been infected.

In a world where people are continually bombarded by the marketing mantra that more is better, rest assured that when it comes to the immune system, maintaining perfect balance is just right.

This edited article is republished from The Conversation under a Creative Commons license. Read the original article.