New research published in Allergyindicates that certain environmental exposures may affect a child’s risk of developing atopic eczema, a condition characterised by dry, itchy, and inflamed skin. In other words, although some people may be genetically predisposed to eczema, certain environmental factors may increase or decrease that risk.
For the study, investigators analysed data from 16 European studies to test for interactions between the 24 most significant eczema-associated genetic variants and 18 early-life environmental factors. They applied their findings to an additional 10 studies and used lab modelling tests to assess their results.
The first analysis (including 25 339 individuals) showed suggestive evidence for interaction between 7 environmental factors (antibiotic use, cat ownership, dog ownership, breastfeeding, elder sibling, smoking, and washing practices) and at least one established genetic variant for eczema, with 14 interactions in total.
In the additional analysis (254 532 individuals), dog exposure interacted with a particular genetic risk variant on chromosome 5, near the gene that codes for the interleukin-7 receptor, a protein involved in immune cell function. Lab modelling tests showed that this variant affects expression of interleukin-7 receptor in human skin cells and that dog exposure modifies the genetic effect of this variant on the development of eczema, essentially providing a protective effect by suppressing skin inflammation.
Additional studies are needed to explore these lab findings and the other potential interactions identified in the first analysis.
“Our research aims to answer some of the most difficult questions that I am asked in clinic: ‘Why does my child have eczema?’ and ‘What can I do to help protect my baby?’ We know that genetic make-up affects a child’s risk of developing eczema and previous studies have shown that owning a pet dog may be protective, but this is the first study to show how this may occur at a molecular level,” said corresponding author Sara J. Brown, MD, PhD, FRCPE, of the University of Edinburgh. “More work is needed, but our findings mean we have a chance to intervene in the rise of allergic disease, to protect future generations.”
A decade ago, a clinical trial in the UK famously showed that children who were exposed to peanuts in the early months of life had reduced risk of developing a peanut allergy compared with children who avoided peanuts.
Now, researchers at Memorial Sloan Kettering Cancer Center (MSK) have a likely answer as to why that’s the case: Thetis cells.
This recently discovered class of immune cells, which were first described by MSK researchers in 2022, plays an essential and previously unknown role in suppressing inflammatory responses to food, according to findings published in Science, one of the world’s premier scientific journals.
Moreover, the study, which was conducted in mouse models, points to a critical window in the early months of life for training the immune system not to overreact to food allergens, termed “oral tolerance.”
The study also opens the door to new therapeutic possibilities, the researchers say.
“This is a great example of how clinical studies can reveal clues to fundamental mechanisms in biology,” says physician-scientist Chrysothemis Brown, MBBS, PhD, the study’s senior author. “These new understandings can pave the way for new treatment strategies for food allergies, which are desperately needed.”
Thetis Cells Train the Immune System To Tolerate Helpful Outsiders
Thetis cells are a type of antigen-presenting cell, whose job is to present foreign substances (antigens) to other immune cells. Antigen-presenting cells must educate the immune system. These cells provide signals that tell the immune system to attack foreign bacteria and viruses – or instruct it to tolerate harmless proteins in the foods we eat.
Previous research led by Dr Brown and immunologist Alexander Rudensky, PhD, Chair of the Immunology Program at MSK’s Sloan Kettering Institute, identified a window in early life where a “developmental wave” of Thetis cells within the gut creates an opportunity for developing immune tolerance.
“We previously showed that Thetis cells train the immune system not to attack the helpful bacteria in the digestive system. So we wondered whether these cells might also be important for preventing inflammatory responses to food, and whether the increased abundance of the cells during early life would result in increased protection against food allergy,” says Dr. Brown, whose lab is in MSK’s Human Oncology and Pathogenesis Program (HOPP).
The new study found that Thetis cells not only help to broker peace accords with “good” bacteria, but also with proteins in foods that can act as allergens, such the Ara h proteins found in peanuts (though they weren’t specifically tested in the study) or the ovalbumin found in eggs.
Thetis cells got their name because they share traits with two different types of antigen-presenting cells: medullary thymic epithelial cells and dendritic cells, just as Thetis in Greek mythology had shape-shifting attributes.
A Key Role for Gut-Draining Lymph Nodes
The research team used a variety of genetically engineered mouse models to investigate oral tolerance. They attached a fluorescent dye to ovalbumin in order to visualise which cells in the gut interacted with it.
And this showed that a subset of Thetis cells, the same ones that regulated tolerance to healthy gut bacteria, took up the protein. This allowed Thetis cells to program another type of immune cell called regulatory T cells to suppress the immune response to the egg protein, essentially telling the body it was safe.
“This process is often studied in adult models, but by examining what happens when mice first encounter food proteins at the time of weaning, we could see which specific cells were critical to generating tolerance to food during early life,” Dr. Cabric says.
Although Thetis cells could also induce tolerance throughout life, there was a significant difference in the immune response when the egg protein was introduced later.
A previously uncharacterised subset of immune cells may play a critical role in the development of allergic diseases and explain differences between urban and rural populations. The finding, published in the journal Allergy, provides new insight into how the immune system is shaped in early life – and why urban children are more prone to allergies than children from rural areas.
Led by researchers from the University of Rochester Medical Center (URMC) Department of Pediatrics, including MD/PhD student Catherine Pizzarello and senior author Kirsi Järvinen-Seppo, MD, PhD, the study uncovered a unique subpopulation of T cells known as helper 2 (Th2) cells with distinct molecular characteristics.
T-cells are the foundational immune cells that fight off infections, but there is evidence that this specific subtype is recognizing certain foods as allergenic and attacking them, according to Jarvinen-Seppo.
“These pro-allergic T cells are more inflammatory than anything previously described in this context,” said Järvinen-Seppo, chief of Pediatric Allergy and Immunology at UR Medicine Golisano Children’s Hospital. “They were found more frequently in urban infants who later developed allergies, suggesting they may be a predictive biomarker or even a mechanistic driver of allergic disease.”
The study compared blood samples from urban infants with those from infants in a farming community, specifically the Old Order Mennonites (OOM) of New York’s Finger Lakes region – known for their low rates of allergies. Researchers found that while urban infants had higher levels of the aggressive Th2 cells, OOM infants had more regulatory T cells that help keep the immune system in balance and reduce the likelihood of allergic responses.
While additional research is needed to identify a possible cause, Jarvinen-Seppo speculates that differences in the development of the gut microbiome between the two populations, and more exposure to “healthy” bacteria in rural children, may be a factor.
“The farming environment, which is rich in microbial exposure, appears to support the development of a more tolerant immune system. Meanwhile, the urban environment may promote the emergence of immune cells that are primed for allergic inflammation,” said Jarvinen-Seppo.
The work is part of a broader, NIH-funded investigation into how early-life exposures influence long-term immune outcomes. In 2023, Järvinen-Seppo’s team received a $7 million grant from the National Institute of Allergy and Infectious Diseases (NIAID) to study environmental, microbiome, and immune differences between OOM and urban infants. The goal is to continue this foundational work to uncover protective factors that could be translated into preventive therapies, including probiotics or microbiome-supporting interventions.
“If we can identify the conditions for this disparity between the different T cell subpopulations, we can potentially find solutions in allergic disease development,” Järvinen-Seppo said.
A review published in The Laryngoscope indicates that climate change’s effects on pollen seasons and concentrations are contributing to increasing rates of allergic rhinitis.
When investigators assessed research published between 2000 and 2023, they identified 30 studies that reported on the current epidemiological state of allergic rhinitis, described factors related to climate change, and observed how global warming is affecting pollen seasons and allergy symptoms.
Sixteen studies reported longer pollen seasons and/or higher pollen concentrations related to climate change. As an example, total pollen emissions in the U.S. are projected to increase by 16–40% by the end of the century and pollen season length to increase by 19 days. Four studies reported an increase in allergic rhinitis–related health care usage, particularly among low-income residents. Two studies reported that health care professionals want more education on climate change.
“Physicians are uniquely positioned to witness the impact of allergic rhinitis on patient outcomes and can adapt their practice as climate change intensifies,” said corresponding author Alisha R. Pershad, BS, a third-year medical student at the George Washington University School of Medicine and Health Sciences. “As trusted voices in the community, they should leverage their frontline experience to advocate for meaningful change in addressing the climate crisis.”
A review in Clinical & Experimental Allergy concludes that exposing young children to small amounts of foods that they’re allergic to is safer than avoiding the foods altogether, which could be very dangerous if accidental exposure occurs.
The review notes that exposing preschool-aged children to small amounts of food allergens—called oral immunotherapy—can lessen the severity of a reaction following an accidental exposure. Also, delaying exposure until a later age misses the window of opportunity when oral immunotherapy is safest, and it prolongs unnecessary dietary restrictions. Also, after early childhood avoidance, some people who outgrow their allergy will not reincorporate the food into their diet due to fear and anxiety, thus potentially increasing their chance of redeveloping the allergy.
A growing body of evidence indicates that oral immunotherapy is safe and effective in preschoolers, but additional research is needed to clarify its impact on children’s health and quality of life.
“This research highlights a critical shift in how we approach food allergies—moving from strict avoidance to controlled exposure in early childhood, which not only reduces the risk of severe reactions but also helps prevent long-term negative consequences of living with food allergies,” said corresponding author Lianne Soller, PhD, of the University of British Columbia, in Canada.
Children with high-threshold peanut allergy who ate gradually larger doses of store-bought peanut butter achieved significantly higher and long-lasting rates of desensitisation compared to those who avoided peanuts, according to a new study led by researchers at the Icahn School of Medicine at Mount Sinai.
“Our study results suggest a safe, inexpensive and effective pathway for allergists to treat children with peanut allergy who can already tolerate the equivalent of at least half a peanut, considered a high-threshold peanut allergy,” said Scott Sicherer, MD, director of a food allergy institute at Mount Sinai and lead author of the paper. “Our findings open the gateway to personalised threshold-based treatments of food allergy and will encourage additional studies that delve deeper into peanut and other foods for this approach that might be a game-changer for the majority of people with food allergies.”
The most common approach to a food allergy is to avoid the food, but in recent years peanut oral immunotherapy – medically supervised, very gradual daily feeding of increasing amounts of pharmaceutical-grade peanut protein – has become an option for individuals with peanut allergies.. However, studies that led to Food and Drug Administration approval of an injected biologic and oral peanut immunotherapy have specifically focused on people who react to very small amounts of food allergens, such as half a peanut or less (considered a low-threshold peanut allergy).
“Years ago, when people with milk and egg allergies were advised to undertake strict avoidance, our team initiated studies that found most people with milk and egg allergies could tolerate these foods in baked goods, which changed the global approach to these allergies,” said Julie Wang, MD, Professor of Pediatrics at the Icahn School of Medicine, clinical researcher at the Jaffe Food Allergy Institute, and co-senior author of the paper. “The research team recognised that more than half of people with peanut allergy can tolerate half a peanut or more, and thought that this group of people might be treatable if we took a different approach to peanut oral immunotherapy. We were thrilled to find that this treatment strategy was even more successful than we had anticipated.”
To test this hypothesis, the study team recruited 73 children ages 4 to 14 years old. Study participants were assigned, at random, to either test the new treatment strategy or continue avoiding peanuts. The children in the peanut-ingestion group began with a minimum daily dose of 1/8 teaspoon of peanut butter and gradually increased their dose every eight weeks over the course of 18 months, ending at one tablespoon of peanut butter or an equivalent amount of a different peanut product. All dose increases took place under medical supervision. None of the study participants in the peanut-ingestion group had severe reactions or needed epinephrine during home dosing and only one received epinephrine during a supervised dosing visit.
Following the treatment regimen, children from the peanut-consuming cohort participated in a feeding test, carefully supervised by the study team, to evaluate how much peanut they could eat without an allergic reaction. All 32 children from the peanut-consuming group who participated in the feeding test could tolerate the maximum amount of 9 grams of peanut protein, or three tablespoons of peanut butter. By contrast, only three of the 30 children from the avoidance group who underwent the feeding test after avoiding peanuts for the duration of the study could tolerate this amount.
Because the trial took place during the COVID-19 pandemic and some families preferred avoiding close encounters indoors, some did not return to the study site for the feeding test. Using a common statistical technique to account for the children who missed the feeding test, the team reported that 100 percent of the ingestion group and 21 percent of the avoidance group tolerated an oral food challenge that was at least two doses more than they could tolerate at the beginning of the study.
To test if the response to treatment was durable, children in the peanut-ingestion group who could tolerate nine grams of protein during the feeding test went on to consume at least two tablespoons of peanut butter weekly for 16 weeks and then avoided peanuts entirely for eight weeks. Twenty-six of the 30 treated children who participated in a final feeding test after the eight-week abstinence period continued to tolerate nine grams of peanut protein, indicating that they had achieved sustained unresponsiveness to peanuts. The three participants from the avoidance group who could eat nine grams of peanut protein without reaction at the earlier food test were considered to have developed natural tolerance to peanuts. A comprehensive analysis of data collected from all 73 study participants revealed that 68.4 percent of the peanut-ingestion group achieved sustained unresponsiveness, while only 8.6 percent of the avoidance group developed a natural tolerance.
“These study results are very exciting and a huge step forward in personalizing food allergy treatment,” concluded Dr. Sicherer, the Elliot and Roslyn Jaffe Professor in Pediatric Allergy and Immunology at Mount Sinai. “My hope is that this study will eventually change practice to help these children and encourage additional research that includes this approach for more foods.”
In addition to expanding the work to more foods and validation studies of their approach, the Mount Sinai study team aims to determine a better way of identifying individuals with higher thresholds, because the best way to do so currently requires a feeding test that is bound to cause an allergic reaction.
How the gut decides which food to tolerate and which food to respond to as an allergen has long puzzled scientists. Now, new research identifies specific gut cell types that communicate with T cells – prompting them to tolerate, attack, or simply ignore – and explains how these opposing responses are triggered.
The findings, published in Science, give scientists a new understanding of how the intestinal immune system keeps the gut in balance, and may ultimately shed light on the root causes and mechanisms of food allergies and intestinal diseases.
“The big question is, how do we survive eating?” says lead author Maria C.C. Canesso, a postdoctoral fellow in the laboratories of Daniel Mucida and Gabriel D. Victora. “Why do our bodies normally tolerate food, and what goes wrong when we develop food allergies?”
Gut decisions
The intestinal immune system is complicated machinery. Tolerance to food begins with antigen presenting cells, or APCs, instructing T cells to stand down. This signal gives rise to pTregs, a special type of T cell that calms the immune response to food particles, and kicks off a cascade of activity involving additional immune cells that reinforce the message. But without knowing which specific APCs run the show, it’s difficult to tease out the ins and outs of the body’s eventual tolerance to food and intolerance to pathogens.
“There are so many types of antigen-presenting cells,” Canesso says. “Pinpointing which ones are doing what is a longstanding technical challenge.”
She began exploring this conundrum as a PhD student in the Mucida lab, which focuses on how the intestine balances defense with tolerance. During her postdoc, Canesso also joined the Victora lab, which developed a technology known as LIPSTIC that helps scientists catalogue cell-to-cell interactions, particularly among immune cells.
“The technological advances made by the Victora lab allowed us to understand immune cell dynamics that would not have been possible using existing tools,” says Mucida, head of the Laboratory of Mucosal Immunology.
After optimising LIPSTIC for the task, Canesso and colleagues succeeded in pinpointing those APCs that promote tolerance – a process primarily handled by two types: cDC1s and Rorγt+ APCs. These cells capture dietary antigens from ingested food and present them to T cells, giving rise to the pTregs that ensure food tolerance.
“When we first developed LIPSTIC, we were aiming to specifically measure the interactions between B and T cells that promote antibody responses to vaccines,” says Victora, head of the Laboratory of Lymphocyte Dynamics. “It was to Maria’s credit that she was able to adapt this to settings so different from those it was originally intended for.”
They also uncovered how infections of the intestines can cause interference, demonstrating in mice that the parasitic worm Strongyloides venezuelensis shifts the balance away from tolerance promoting APCs and toward those that promote inflammation. Indeed, mice infected with this worm during a first exposure to a dietary protein display reduced tolerance towards this protein, and signs of allergy when challenged.
Finally, the team characterised the molecular signals underpinning these immune shifts, identifying key cytokines and pathways that influence how APCs present antigens and modulate immune responses. For example, the infection induced a surge in pro-inflammatory cytokines such as IL-6 and IL-12, which have been shown to nudge APC activity toward inflammatory outcomes. This inflammatory environment appears to override the immune system’s tolerance mechanisms. “The worm infection induces this an expansion of non-tolerogenic APCs that help deal with the infection, outnumbering the tolerance-related APCs,” Canesso says.
From food to food allergies
Together, the findings illuminate how the immune system maintains food tolerance and, in the case of parasitic infections, highlights the specific immune mechanisms that can go awry. “It’s important to note that our findings do not suggest that worm infections trigger food allergies,” clarifies Mucida, head of the Laboratory of Mucosal Immunology. “They reduce tolerance mechanisms while the immune response focuses on dealing with the worms.”
While these findings aren’t directly relevant to food allergies, they do lay some groundwork for further investigation into food intolerance. “If food allergies are derived from dysregulation on intestinal APCs inducing tolerance and protective responses to infections, perhaps we could one day modulate those APCs specifically to prevent food allergies,” Canesso says.
Next up, Canesso plans to shift her focus toward early life, exploring how maternal-neonatal interactions shape food intolerance. “Most allergies develop early in life,” she says. “I want to focus on how breast milk and maternal exposure to dietary antigens may influence a baby’s immune system, potentially shaping their risk of developing food allergies.”
Photo by Mariana Kurnyk: https://www.pexels.com/photo/two-baked-breads-1756062/
A research team led by the University of Nottingham has used magnetic resonance imaging (MRI) to better understand the impact a gluten free diet has on people with coeliac disease, which could be the first step towards finding new ways of treating the condition.
Coeliac disease is a chronic condition affecting around one person in every 100 in the general population. When people with coeliac disease eat gluten, which is found in pasta and bread, their immune system produces an abnormal reaction that inflames and damages the gut tissue and causes symptoms such as abdominal pain and bloating.
The only treatment is a life- long commitment to a gluten free diet, which helps recovery of the gut tissue but still leaves many patients with gastrointestinal symptoms.
Luca Marciani, Professor of Gastrointestinal Imaging at the University, led the study. He said: “Despite being a common chronic condition, we still don’t precisely know how coeliac disease affects the basic physiological functioning of the gut and how the gluten free diet treatment may further change this.
“We launched the MARCO study to try and address this issue, by using MRI along with gut microbiome analysis to give us new insights into how a gluten-free diet affects people with coeliac disease.”
The team recruited 36 people who had just been diagnosed with coeliac disease and 36 healthy volunteers to participate in the study. Images were taken of their guts with MRI, along with blood and stool samples. The patients then followed a gluten free diet for one year and came back to repeat the study. The healthy participants came back one year later too and repeated the study, but they did not follow any diet treatment.
The study found that the newly diagnosed patients with coeliac disease had more gut symptoms, more fluid in the small bowel and that the transit of food in the bowel was slower than in the healthy controls.
The microbiota (the ‘bugs’ living in the colon) of the patients showed higher levels of ‘bad bugs’ such as E.coli. After one year of a gluten free diet, gut symptoms, bowel water and gut transit improved in the patients, but without returning to normal values. But the gluten free diet also reduced some of the ‘good bugs’ in the microbiota, such as Bifidobacteria associated with reduced intake of starch and wheat nutrients, due to the different diet.
The patient study was conducted by Radiographer Dr Carolyn Costigan, from Nottingham University Hospitals, as part of her PhD studies at the University of Nottingham.
It was particularly interesting to see how the imaging results on gut function correlated with changes in the ‘bugs’ in the colon microbiota. The findings increase our understanding of gut function and physiology in coeliac disease and open the possibility of developing prebiotic treatments to reverse the negative impact of the gluten free diet on the microbiome.”
Luca Marciani, Professor of Gastrointestinal Imaging
Dr Frederick Warren from the Quadram Institute, which contributed to the research, said: “This study is the result of an exciting and innovative research collaboration bringing together medical imaging technology and gut microbiome analysis. We provide important insights which pave the way for future studies which may identify novel approaches to alleviate long-term symptoms in coeliac patients.”
Individuals at risk of anaphylaxis are often prescribed adrenaline (epinephrine) autoinjectors such as EpiPens. A recent review published in Clinical & Experimental Allergy finds that these autoinjectors, which people use to self-administer adrenaline into the muscle, can deliver high doses of adrenaline into the blood, but these levels are short-lived and may not be sufficient to save lives in cases of fatal anaphylaxis.
Anaphylaxis is an acute systemic hypersensitivity reaction to an allergen or trigger, typically associated with skin reactions, nausea/vomiting, difficulty breathing, and shock.
Investigators noted that data from animal and human studies suggest that intravenous adrenaline infusions delivered directly into the blood can prevent fatal anaphylaxis, but adrenaline autoinjectors may have little impact in such deadly cases.
“For effective management of the most severe allergic reactions, adrenaline given by continuous intravenous infusion, with appropriate fluid resuscitation, is likely to be required—how this is safely achieved in the pre-hospital setting remains to be determined,” the authors wrote. This challenge stems from the fact that fatal anaphylaxis is unpredictable and fast. Fortunately, fatality is rare, with a population incidence of 0.03–0.51 per million per year.
Researchers at the University of Bern and Bern University Hospital have developed a test to simplify the diagnosis of allergies by testing mast cells. Its effectiveness has now been confirmed in clinical samples from children and adolescents suffering from a peanut allergy. The results, recently published in the European Journal for Allergy and Clinical Immunology (Allergy), could fundamentally improve the clinical diagnosis of allergies in future.
Food allergies are a major health problem worldwide. In some countries, up to 10% of the population is affected, mainly young children. Peanut allergy, in particular, is one of the most common diseases and often manifests itself in severe, potentially life-threatening reactions. The stress of food allergies not only affects the individuals concerned, but also has far-reaching consequences for their families, the health system and the food industry. The oral food challenge test, in which people consume the allergen (such as peanut extract) under supervision to test the allergic reaction, is still considered the gold standard in diagnosis. However, the method is complex and carries health risks. The allergen skin prick test and blood test are often not very accurate, which can lead to misdiagnoses and unnecessary food avoidance.
A team of researchers led by Prof Dr Alexander Eggel and Prof Dr Thomas Kaufmann from the University of Bern, developed an alternative test in 2022. It mimics the allergic reaction in a test tube and thus offers an attractive alternative to standard tests. The Bern researchers have now investigated the effectiveness of the test on samples from children and adolescents with confirmed peanut allergy and a healthy control group in a clinical study in collaboration with partners from the Hospital for Sick Kids in Toronto, Canada. They were able to show that the new test has a higher diagnostic accuracy than the methods used so far.
Mast cell activation test as appropriate alternative
“The most common food allergies are type I allergies. They develop when the body produces immunoglobulin E (IgE) antibodies in response to substances that are actually harmless (allergens),” explains Alexander Eggel. These antibodies bind to specific receptors on the mast cells, which are immune cells that play an important role in allergic reactions and inflammation. They are mainly located in the tissue, for example, in the intestinal mucosa, and are prepared for and sensitised to the allergen by binding to the antibodies. Upon renewed contact with the allergen, it binds directly to the mast cells loaded with antibodies, activating them and triggering an allergic reaction.
“In the Hoxb8 mast cell activation test (Hoxb8 MAT), which we developed, mast cells grown in the laboratory are brought into contact with blood serum from allergic patients. The mast cells bind the IgE antibodies from the serum and are sensitised by them. We can then stimulate the mast cells with different amounts of the allergens to be tested,” says Eggel. Quantifying the activated mast cells suggests how allergic a patient is to the allergen tested without needing to consume the food.
Higher diagnostic accuracy than standard tests
The study used serum samples from a total of 112 children and adolescents who had already participated in a study in Canada and for whom clear diagnostic data on their peanut allergy status were available. The mast cells cultured in the laboratory were sensitised with their serum and then stimulated with peanut extract. “The cell-based test was easy to carry out and worked perfectly. All samples were measured within two days, which was very fast,” says Thomas Kaufmann. The results showed that a large number of sera from allergic patients exhibited allergen dose-dependent activation, while almost all samples from the non-allergic control subjects did not activate the mast cells. “An exceptionally high diagnostic accuracy of 95% could be calculated from these data,” Eggel adds.
In addition, the data measured in the study were analysed in direct comparison with other diagnostic methods established at the hospital. It was found that the Hoxb8 MAT test had significantly higher accuracy than the standard measurement of allergen-specific IgE antibodies in the blood or the frequently used skin test. “Comparison with other clinical tests was crucial to determine which of them reflected the patients’ allergic reaction best. The new mast cell activation test has the advantage that it is functional and therefore incorporates many parameters that are important for triggering the allergy,” says Thomas Kaufmann, adding: “The new test is also based on stable blood serum, which can be drawn using simple blood sampling and then stored in the freezer. This eliminates the challenging logistical obstacles that arise with other methods.” The study also showed that the Hoxb8 MAT test leads to less false negative results.
“What has been shown in this study on the diagnosis of peanut allergies can also be applied to other allergies in a simple way. The technology is a perfect example of how basic research from the University of Bern can be brought to the clinical practice, and might ultimately simplify life for patients and physicians,” concludes Eggel.
