A hidden molecular defect in inflammatory bowel disease may help explain why flare-ups can return even when patients appear well. Even when inflammatory bowel disease appears under control, intestinal cells may remain primed to die. In a WEHI-led study, researchers found this hidden molecular defect in patients with few or no symptoms, and higher levels [...]
The patient: A 47-year-old woman in Canada
The symptoms: The woman underwent a lung transplant to treat interstitial lung disease, which involves harmful inflammation and scarring of lung tissue. While recovering in the hospital, she ate a bowl of breakfast cereal, which activated a nearly two-hour episode of flushing, itching, shortness of breath and low blood pressure.
This severe, life-threatening allergic reaction is known as anaphylaxis. A report of the woman's case does not mention specific treatment she received for this reaction, but it notes that it resolved after two hours.
(Treatment for anaphylaxis involves epinephrine (also called adrenaline), and it can also require antihistamines, cortisone, oxygen and beta-agonists, such as albuterol, which help improve breathing.)
What happened next: The woman experienced the same symptoms in the weeks after being discharged from the hospital — after eating a coconut cream pie and after having an almond candy bar.
The diagnosis: Two months after her lung transplant, the woman underwent a skin-prick allergy test, which revealed a sensitivity to peanut and pine nut allergens. She did not have an allergic response to tree nuts, such as the almonds in the candy bar, nor to coconut. None of the foods that triggered her symptoms were known to contain peanuts, but none were certified as peanut-free, either.
Notably, the woman's lung donor had been a 12-year-old boy with a known peanut allergy but no history of anaphylaxis. Her doctors theorized that the transplanted lung tissue contained immune cells from the donor that were sensitized to nut allergens.
The treatment: The woman did not receive a specific treatment to get rid of this new allergic response. However, the sensitivity subsided in follow-up skin-prick tests, and they had disappeared completely by a year after her surgery. She ate peanuts in a supervised setting a few months after the one-year mark and had no reaction.
The doctors reasoned that the sensitized immune cells from the donor must have cleared from her body.
What makes the case unique: Only one other case of peanut allergy following a lung transplant had been documented before the woman's case was published in 2011.
Scientists had only recognized the risk of allergies being passed from organ donors to recipients a little over a decade before the report, according to a 2025 review of such instances. Doctors had previously reported allergy transfer linked to bone marrow transplants, which makes sense given that bone marrow produces immune cells. But the first known donor-acquired allergy from a solid-organ transplant was observed in 1997 following a combined kidney-liver transplant from a donor who was allergic to peanuts.
The authors of the 2025 review noted that donor-acquired allergies are more commonly associated with lung and liver transplants than with transplants of other solid organs. That could be because these organs are rich in a type of immune cell that produces allergen-specific antibodies, called B lymphocytes.
Other potential culprits for donor-acquired allergies are mast cells and basophils, two types of immune cell that bind to those allergen-specific antibodies. The cells hold onto the antibodies, and when they encounter an allergen, they release the inflammatory compounds responsible for anaphylaxis.
In the woman's case, a blood test for peanut-specific antibodies came back negative. This suggested that her body was not continually generating the antibodies. That could serve as possible evidence that her reaction was caused by antibodies bound to mast cells or basophils within the donor tissue, rather than antibodies produced by lymphocytes.
That said, the woman's reaction to the skin-prick test could imply that lymphocytes were still involved in the allergic reaction, the doctors added, as they did not know whether mast cells or basophils could migrate to the skin the way circulating antibodies could.
Regardless of the cell type behind the woman's peanut allergy, the sensitivity faded after a year, consistent with other cases described in the 2025 review. Still, the review authors called for better donor allergy labels to inform allergy testing and treatment for organ recipients. The doctors in the case report came to a similar conclusion, noting that detailed donor allergy histories and skin-prick testing after organ transplant could help identify donor-acquired allergies.
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.
Bat DNA may hold clues to a long and healthy life, according to an international team of researchers.
These small creatures grace the night skies with extremely long lifespans and low cancer rates—traits that may ultimately benefit humanity if scientists can figure out how bats achieve them. Now, in a recent paper published in Nature, scientists from the University of Vermont and Penn State University led an international team investigating bats’ immune systems.
The paper’s crucial discovery was that bat DNA reveals the creatures encode genomic changes to handle exposure to environmental pathogens.
“Pathogen adaptation, longevity, and cancer resistance—they are fundamentally linked,” explained co-lead author Elise Lauterbur, an assistant professor of evolutionary biology at the University of Vermont. “Many of the genes that have adapted to viruses in bats are genes that are also involved in longevity and cancer resistance.”
Bats make an ideal study subject as they are only second to rodents in diversity, allowing scientists to study a wide variety of features in a single order.
“If you look at two bats, the same size, one lives 3 years the other lives 30 years and they are very closely related, like humans and Neanderthals, you can essentially find a very small number of genetic changes that leads to a very big change in their lifespan,” said co-lead author Juan Manuel “Manny” Vazquez, an assistant professor at Penn State University. “And that is kind of the Holy Grail for evolutionary medicine.”
The work focused on Myotis, one of the largest bat genera, whose members are found across much of the globe outside Antarctica. Eight Myotis species came under the microscope, with the team experimenting on cultured cells and analyzing their genomes. Among the species sampled were little brown bats (Myotis lucifugus), known both for their long lifespans, even among bats, and their susceptibility to the deadly white-nose syndrome, a fungal disease.
Even the researchers’ sample-collection methods were novel. They developed a technique akin to ear-piercing to collect small tissue samples from bat wings, which were then used to establish cell cultures. The team says this both spared the animals’ lives and produced more scientifically useful samples.
In their detailed examination, the researchers identified evidence of past events in which Myotis bats encountered pathogens and how adaptations to those viruses were selected for during their evolution.
Their work identified specific genomic changes, including the duplication or deletion of genes, associated with adaptation to environmental pathogens. This illuminated important differences in bats’ responses to DNA and RNA viruses compared with humans and other primates, potentially contributing to bats’ long, healthy lifespans.
Comparatively, human evolution shows stronger selection involving proteins that interact with RNA viruses like influenza, while bats show stronger selection involving proteins that interact with DNA viruses such as herpesviruses. These differences may help explain the distinct ways bats and primates have adapted to viral threats.
The team also identified genetic mechanisms that could help explain bats’ resistance to cancer and other age-related diseases. In some cases, duplicated genes can diversify their functions, allowing different copies to perform distinct roles. According to the researchers, this may provide immune advantages that help bats combat multiple viruses while also contributing to pathways associated with longevity.
Another important finding was that while most mammals contain one copy of the immune-related gene PRKN, some bat species contain two or even three copies, suggesting that additional copies may offer evolutionary advantages. The team says this could provide important insights for future cancer research, given bats’ unusual ability to repair or eliminate damaged cells.
The research doesn’t point to immediate treatments for humans, but it does provide starting points for reconsidering human illness in the context of bat immunology and evolution.
“Everything is connected,” Vazquez concluded. “Everything uses the same shared set of biology. … We don’t have to treat all of these different problems as silos. We can now start focusing on systems like bats to understand how we can solve multiple human age-related diseases.”
The paper, “Insights into Longevity and Virus-Driven Adaptation from Myotis Bat Genomes,” appeared in Nature on August 26, 2026.
Ryan Whalen covers science and technology for The Debrief. He holds an MA in History and a Master of Library and Information Science with a certificate in Data Science. He can be contacted at ryan@thedebrief.org, and follow him on Twitter @mdntwvlf.
How immune cells develop and retain memory may work differently than medical scientists previously believed, according to an international team of researchers.
The new work shows that T cells—white blood cells essential to immune function—can respond to the physical properties of their surroundings through a kind of cellular sense of touch.
The researchers published the work in Nature Immunology, altering our understanding of how immune cells develop, and potentially improving scientists’ understanding of how the immune system adapts to the varied physical environments found throughout the human body.
The various specialized types of T cells serve crucial roles in the immune system. Some directly fight infections, while others help coordinate the immune response. Scientists have long believed that biochemical signals help shape the memory T cells that persist in tissues following an infection, preserving the body’s ability to respond to previously encountered threats. How these cells migrate and eventually settle into strategic positions throughout the body is a key part of the immune response.
As T cells travel through the body, they continually monitor for signs of pathogens. When a threat is detected, T cells can enter affected tissues and help clear the infection. Once the invaders have been repelled, some T cells remain in the tissue to guard against reinfection. These tissue-resident memory T cells help defend against previously encountered threats but can also play roles in autoimmune disorders and the rejection of transplanted tissue.
Over their lifetimes, T cells can develop into increasingly specialized forms. Naive T cells have not yet encountered the specific antigen they are capable of recognizing. Following activation, they can differentiate into effector T cells that help target a particular threat, with some eventually developing into long-lived memory cells.
Tissues in our bodies vary widely in stiffness, ranging from the very soft adipose tissue that makes up our body fat to the much stiffer skeletal muscle tissue. These differences raise an interesting question: how do T cells remain strong enough to survive the pressures of stiffer tissues while staying soft enough to change shape as they slide through obstacles in our bodies?
For their laboratory experiments, the researchers reproduced typical tissue stiffnesses using specially engineered collagen gels. They then placed human and mouse immune cells into the gels and discovered that T cells were more likely to develop characteristics associated with tissue-resident memory cells in stiffer environments.
Previously, scientists believed biochemical signals were the primary driver of tissue-resident memory T cell development. In their new research, the team found that these cells use touch to sense the mechanical pressure of their surroundings, dictated by tissue stiffness, and adjust their morphology to compensate.
“This is an exciting fundamental finding that challenges the way we think about immune cells,” said lead author Judith Mandl, a professor in McGill University’s Department of Physiology. “It suggests T cells can ‘feel’ their surroundings and adapt to them, making the physical environment an active force in shaping their behaviour.”
While T cells normally function to protect us from illness, they can occasionally create problems of their own. Patients with autoimmune diseases and allergies may see these immune cells begin attacking healthy tissue. Additionally, organ transplant patients typically require immunosuppressant drugs to stop their T cells from rejecting the new organ.
“Tumours are often dense and physically difficult for immune cells to penetrate. Understanding how T cells adapt to these environments could help researchers design cancer immunotherapies that are better able to reach and attack tumours,” said Mandl.
This new research is an important first step in a new understanding of how immune cells differentiate, which could lead to a new foundational understanding of how to correct undesired immune responses.
The paper, “Mechanosensing by T Cells Promotes a Tissue-Resident Memory Transcriptional Program,” appeared in Nature Immunology on July 3, 2026.
Ryan Whalen covers science and technology for The Debrief. He holds an MA in History and a Master of Library and Information Science with a certificate in Data Science. He can be contacted at ryan@thedebrief.org.
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