Publisher Health

Doing less exercise could deactivate a vital protein in the body, causing further inactivity and making exercise more difficult, new research suggests.
University of Leeds scientists have discovered that deactivating the Piezo1 protein, a blood flow sensor, reduces the density of capillaries carrying blood to the muscles.
This restricted blood flow means activity becomes more difficult and can lead to a reduction in how much exercise is possible, the team found.
They say the results help to explain the biology of why exercise becomes harder the less you do.
The paper, Endothelial Piezo1 sustains muscle capillary density and contributes to physical activity, is published today in Journal of Clinical Investigation.
The experiments were carried out in mice, but the Piezo1 protein is found in humans, suggesting the same results could occur.

New research from the University of East Anglia (UEA) and Quadram Institute reveals how our immune system can be triggered to attack cancer cells.
The research, published today in the Journal of Clinical Investigation, could help develop new approaches to treating people with leukaemia.
The team studied acute myeloid leukaemia — a blood cancer which is very difficult to treat.
The research was led by Dr Stuart Rushworth from UEA’s Norwich Medical School, in collaboration with Quadram Institute, Earlham Institute and the Norfolk and Norwich University Hospital (UK).
The study identified a process of activating the immune system to fight the leukaemia cells.
The team found that immune cells known as macrophages could be programmed to attack the cancer cells through a protein known as STING (Stimulator of interferon genes), a well-established activator of the immune system.

An ultrasound scan can be used to detect cases of prostate cancer, according to new research.
Researchers at Imperial College London, University College London and Imperial College Healthcare NHS Trust have found that a new type of ultrasound scan can diagnose most prostate cancer cases with good accuracy in a clinical trial involving 370 men.
The ultrasound scans missed only 4.3 per cent more clinically important prostate cancer cases — cancer that should be treated rather than monitored — compared to magnetic resonance imaging (MRI) scans currently used to detect prostate cancer.
MRI scans are expensive and time-consuming. The team believes that an ultrasound scan should be used as a first test in a community healthcare setting and in low and middle income countries which do not have easy access to high quality MRI scans. They say it could be used in combination with current MRI scans to maximise cancer detection. The study is published in Lancet Oncology.
Professor Hashim Ahmed, lead author of the study and Chair of Urology at Imperial College London, said:
“Prostate cancer is the most commonly diagnosed cancer in the UK. One in six men will be diagnosed with the disease in their lifetimes and that figure is expected to rise.

A University of Cincinnati clinical trial that added an immunotherapy drug to standard of care treatment regimens has shown increased survival rates for head and neck cancer patients with intermediate risk features.
Trisha Wise-Draper, MD, led the trial and was the lead author on a paper detailing its findings that was recently published in Clinical Cancer Research, a journal of the American Association for Cancer Research.
Targeting the immune checkpoint
Wise-Draper said the trial focused on adding a drug, pembrolizumab, to patients’ typical standard care of treatments. Pembrolizumab, sold under the brand name Keytruda, is an antibody used in cancer immunotherapy that treats a variety of cancers, including head and neck. The drug targets a pair of receptors that usually work to turn off the human immune system when the immune system has finished a job of fighting off a foreign substance that causes sickness.
“Once the virus or infection is cleared, you have to have a way to turn your own immune system off, to tell it that the infection is gone and it’s time to calm down,” explained Wise-Draper, associate professor of medicine in the Division of Hematology/Oncology in UC’s College of Medicine, Head and Neck Center of Excellence co-leader, medical director of the University of Cincinnati Cancer Center Clinical Trials Office and Lab and a UC Health physician.
Tumor cells have learned to kick the receptors that shut the immune system system off into overdrive, which blocks immune cells from recognizing that tumor cells are foreign objects that the body should attack. Pembrolizumab, however, blocks the interaction and keeps immune cells working, which in turn leads to the immune cells attacking cancerous cells like they are supposed to.

Researchers from two independent research teams have discovered how the mislocalization of a protein, known as TDP-43, alters the genetic instructions for UNC13A, providing a possible therapeutic target that could also have implications in treating amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other forms of dementia. ALS and FTD are two neurodegenerative disorders in which many cases are linked by mislocalization of TDP-43, where instead of being primarily located in the nucleus of the cell where genes are activated, it forms aggregates outside the nucleus in multiple neurodegenerative diseases. Rare mutations in the TDP-43 gene are known to cause ALS, but almost all cases of ALS show mislocalization of TDP-43. The studies were published in Nature.
“ALS and FTD patients have long participated in genetic studies looking for changes in genes that might contribute to risk for disease,” said Thomas Cheever, Ph.D., program director at the National Institute of Neurological Disorders and Stroke (NINDS). “Here, we see two independent research teams converging to explain how one of these changes can be a critical factor contributing to an entire class of neurodegenerative diseases, as well as a potential therapeutic target.”
One study, which is a collaboration between the labs of Michael Ward, M.D., Ph.D., scientist at the National Institutes of Health’s NINDS, and Pietro Fratta, Ph.D., professor at the University College London Queen Square Motor Neuron Disease Centre in the United Kingdom, initially looked at lab-grown neurons derived from human induced pluripotent stem cells (iPSCs) — stem cells created from a patient’s tissue sample, often skin or blood. Using powerful genetic tools, the researchers created neurons that made much less TDP-43 protein than normal, and this resulted in the appearance of abnormal mRNA sequences inserted into the instructions used to make several other proteins. These abnormally inserted sequences, called cryptic exons, can result in a defective protein or can even prevent the protein from being made at all.
The UNC13A gene is important for maintaining the connections between neurons and has been shown to be a risk factor for both ALS and FTD. UNC13A is also one of the mRNA sequences that contained cryptic exons when TDP-43 was reduced, and cryptic exons were also seen in neurons taken from postmortem tissue of ALS and FTD patients. These findings directly link a well-established risk factor for ALS and FTD with the loss of TDP-43.
“We have built on years of genetic research that identified that UNC13A was implicated in motor neuron disease and FTD and supported it with a new molecular biology finding that confirms that the gene is absolutely fundamental to the disease process,” said Dr. Ward.
At the same time, Aaron Gitler, Ph.D., professor at Stanford University in Stanford, California, and his lab, along with a team led by Len Petrucelli, Ph.D., professor at Mayo Clinic in Jacksonville, Florida, were also looking at the effects caused by a loss of TDP-43 as they pertained to FTD and ALS. They first analyzed existing datasets in which postmortem neurons from patients with FTD or ALS were sorted based on whether their nucleus contained TDP-43. When genes were compared between neurons with and without TDP-43, UNC13A again emerged as one that was significantly affected by TDP-43 loss. Knocking down TDP-43 in otherwise healthy cells also introduced cryptic exons into the UNC13A gene, suggesting that this is a direct effect on the gene itself. They also show that the genetic code differences in the variants of UNC13A that are associated with FTD and ALS occur where the cryptic exon is located. It is known that mislocalization of TDP-43 similarly causes cryptic exon splicing into another gene that encodes the protein stathmin 2, which is depleted in the motor neuron and implicated in neurodegeneration. Both studies suggest that developing means to increase the levels of UNC13A or stathmin 2 may be effective in preventing the death of neurons in these tragic disorders.
TDP-43 mislocalization is seen in other degenerative diseases, including Alzheimer’s disease, chronic traumatic encephalopathy (CTE), limbic predominant, age-related TDP-43 encephalopathy (LATE), and inclusion body myopathy, suggesting that these findings could be extended to those conditions as well.
The studies were supported in part by the Intramural Research Program at NINDS, and grants from NINDS (NS097263, NS097273, NS123743, NS084974, NS104437, NS120992, and NS113636) and the National Institute on Aging (AG071326, AG06267, and AG006786).

A new paper in Annals of Neurology describes the approach, structure, and launch of the HEALEY ALS Platform Trial- the first platform trial for amyotrophic lateral sclerosis (ALS) designed to accelerate the development of effective and breakthrough treatments for people with the illness.
“This study is really the first comprehensive platform for ALS drug development, where a central infrastructure is shared between a variety of investigational products, each tested using a common protocol and compared to a shared placebo cohort,” says first author and co-principal investigator Sabrina Paganoni, MD, PhD, co-director of the Massachusetts General Hospital (MGH) Neurological Clinical Research Institute (NCRI), physician scientist at the Healey & AMG Center for ALS at Mass General, and assistant professor of PM&R at Harvard Medical School and Spaulding Rehabilitation Hospital. “Due to this design, people living with ALS who participate in this trial have a greater chance of receiving an active treatment.”
Under the leadership of Paganoni and principal investigator Merit Cudkowicz, MD, MSc, director of the Sean M. Healey and AMG Center for ALS, chief of Neurology at MGH and the Julieanne Dorn Professor of Neurology at Harvard Medical School, the HEALEY ALS Platform Trial enrolls patients across a network of more than 50 coordinated sites of the NEALS Consortium nationwide. The trial simultaneously evaluates several treatments on an ongoing basis.
“The trial has several important scientific goals as we are collecting a number of novel biomarkers and outcome measures which could provide more efficient readouts not only for this trial for the entire ALS clinical trial landscape,” says Cudkowicz. “Further, we are creating an approach that ensures data sharing and sample sharing from the growing placebo cohort where we hope we can contribute to our understanding of the science behind ALS and share the learnings in a collaborative manner.”
Currently, the HEALEY ALS Platform Trial has completed enrollment in its first four trial arms and testing of a fifth investigational product has already begun. “An important feature of the trial is that it will be evergreen, meaning that we intend to always have multiple investigational products available to new participants,” says Paganoni. The team is working with more industry collaborators to create new treatment spots in 2022 with a plan for many more after that.
Since its inception in Summer 2020, more than 800 patients have enrolled in the HEALEY ALS Platform trial, with about 160 participants assigned to the first four trial arms. Results from these first four studies are expected later in 2022. “Because of the platform nature of the study and the use of a shared placebo group, the active to placebo ratio is very favorable for participants, three to one in favor of receiving an active drug,” says Paganoni. “That is simply not possible with traditional stand-alone trials ,” she says. The trial design allows all participants to receive active treatment as part of a long-term Open Label Extension (OLE) after six months of randomized, placebo-controlled trial participation. In addition to granting access to active drug, the OLE will provide important scientific data about the long-term safety and efficacy of the investigational products tested in the trial.
The HEALEY ALS Platform Trial has invigorated the ALS clinical trials landscape, and there has been resounding support from the patient community. Enrollment has been exceeding expectations which is remarkable considering that the trial’s launch coincided with the COVID-19 pandemic.
“We are grateful to the members of our Patient Advisory Committee who have been working with us to design a patient-centric trial with more access opportunities,” says Paganoni. “This trial would not be possible without the generous contributions of hundreds of people with ALS and their families and supporters who decided to devote their time and efforts to ALS research to benefit the entire ALS scientific and patient family during these challenging pandemic times.”
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A multidisciplinary team at the University of Illinois Urbana-Champaign has devised a new approach to 3D imaging that captures DNA methylation, a key epigenetic change associated with learning in the brain. The scientists say their proof-of-concept study in pigs will easily translate to humans, as the new method relies on standard MRI technology and biological markers already in use in human medicine.
Epigenetics is a key mechanism by which gene expression is regulated. The new approach — called epigenetic MRI, or eMRI — will open up new avenues of research into how such changes mold the brain, allowing it to grow, learn and respond to stress, the researchers said. The technique also may be useful in the study of neurodegenerative processes like Alzheimer’s disease.
The findings are reported in the Proceedings of the National Academy of Sciences.
DNA methylation is one mechanism that cells use to regulate which genes are actively expressed, said Dr. King Li, a professor in the Carle Illinois College of Medicine at the U. of I. who led the research with U. of I. bioengineering professor Fan Lam and Gene Robinson, the director of the Carl R. Woese Institute for Genomic Biology at Illinois.
“Our DNA is the same from cell to cell and it doesn’t change,” Li said. “But tiny molecules, like methyl groups, are attached to the DNA backbone to regulate which genes are actively being transcribed into RNAs and translated into proteins. DNA methylation is a very important part of the control of gene functions.”
Previous research showed that DNA methylation is one of several epigenetic changes that occur in the brain when an animal responds to its environment, said Robinson, a professor of entomology at Illinois who studies the interplay of genomics, experience and behavior in honey bees. His studies have shown that many genes in the brain are upregulated or downregulated in bees as they mature, change roles in the hive, encounter new food sources or respond to threats.

Scientists are split over whether the benefits some microdosers experience are a placebo effect or something more.Joseph started microdosing psychedelics five years ago to try to improve his mental health. “I was just kind of in this depression, in this rut,” he said. “I was unhappy and angry and agitated all the time, and it went against the way that I saw myself.”Depression and anxiety run in Joseph’s family, and he’d been prescribed Prozac as a kid. But when symptoms of depression returned in his early 30s, he didn’t want to go back to a prescription drug.Joseph, an Austin-based designer (he asked to withhold his full name, citing privacy concerns surrounding mental health issues and illegal drug use), came across research from Johns Hopkins University about psilocybin, the active ingredient in hallucinogenic, or “magic,” mushrooms. In a small study, full doses of the drug helped cancer patients cope with depression and anxiety. Then he read anecdotes of Silicon Valley influencers claiming increased energy from taking tiny doses of psychedelics. So he decided to start microdosing a few times a week, eating a “small nibble” — about half an inch — of mushrooms to see if it would improve his mood.Almost immediately he started seeing a benefit. “It just kind of boosted my morale,” he said. “I was in a little bit better mood. I had a little bit more pep to my step. I was having a little bit more fun, feeling a little bit more excited about things.”Microdosing is typically defined by experts as taking 5 percent to 10 percent of a full dose of a psychedelic, usually LSD or psilocybin, as a way to get the supposed mental health benefits of the drug without the hallucinogenic high. For instance, in a clinical setting, a 155-pound man might take 20 milligrams of psilocybin for a full psychedelic experience. For a microdose, he’d take only one to two milligrams. At that level, taken several times a week, some claim the drugs improve their mood, boost their creativity and give the world a brighter, shinier quality, like it’s in high-definition.“It’s akin to walking outside and the sun is suddenly out,” said Erin Royal, 30, a bartender in Seattle who microdoses one or two times a week with mushrooms she forages from nearby forests. “It reminds you that you are a person who can feel positive things and notice things that are beautiful.”In practice, only about a third of people who microdose carefully measure the amount of the psychedelic they are taking; most take just enough to begin feeling some effects, which usually start after an hour and last four to six hours. That requires some trial and error — particularly when eating mushrooms, which can vary in psilocybin concentration. (The most commonly reported negative side effect of microdosing is accidentally taking too much, which isn’t dangerous but can be inconvenient if you’re at the office. Researchers also say frequent repeated doses of a psychedelic could theoretically stress the heart.)Research into the mental health benefits of full doses of psychedelics is promising, and one early-phase study even found that psilocybin, at high doses, may be as effective as a selective serotonin-reuptake inhibitor for treating depression. Full doses of psychedelics help the brain develop new cellular connections, a process called neuroplasticity, and there’s some evidence that microdoses produce similar changes.So many of the scientists who pioneered research into full doses of psychedelics have started studying whether a microdose might also be beneficial. But evidence is limited, and experts are divided about how microdosing helps people — or if it does at all.Much of the early research into microdosing has been anecdotal, consisting of enthusiastic survey responses from users who experienced enhanced attention and cognition, feelings of well-being and relief from anxiety and depression. Lab studies of psilocybin and LSD microdoses tend to support these claims, showing improvements in mood, attention and creativity. But these studies have generally been small, and they didn’t compare a microdose to a placebo.“You probably only participate at this point in a trial in microdosing if you really have a strong belief that this might help you,” said Dr. David Erritzoe, clinical director of the Centre for Psychedelic Research at Imperial College London. And when people expect to benefit from a drug, they typically do.The two largest placebo-controlled trials of microdosing were published last year, and they both suggest that the benefits people experience are from the placebo effect. In the studies, volunteers used their own drugs to participate and, unknown to them, received either active doses or a placebo packaged in identical capsules. At the end of several weeks, almost everyone’s mood and well-being had improved, regardless of what they had taken.“I was initially surprised but also a bit disappointed by the results, because when we set up the study we were quite optimistic that microdosing could have an effect” beyond a placebo, said Michiel van Elk, an assistant professor of cognitive psychology at Leiden University in the Netherlands who led one of the trials.Dr. Erritzoe, who ran the other study, found that the drug’s efficacy was tied to users’ expectations. If they took a placebo but thought it was a microdose, they felt better, and if they had an active dose but wrongly guessed it was a placebo, they did not.A third placebo-controlled trial, published earlier this month from the University of Chicago, tried to get around user expectations by giving participants four microdoses of LSD over the course of two weeks, but without telling them about the purpose of the study or even what they were taking. Once again, there was no difference between the LSD and placebo groups.Still, some scientists point to evidence showing that microdosing has a direct impact on the brain to argue that its benefits are real. Using neuroimaging technology, researchers have shown changes in brain activity and connectivity after single small doses of LSD that are similar to what’s seen with larger amounts of the drug. And a study in Denmark found that a microdose of psilocybin activated nearly half of the specific type of serotonin receptors that psychedelics act on to produce their hallucinogenic effects.“I wouldn’t say it’s all placebo. Clearly, it’s an active drug,” said Harriet de Wit, a professor of psychiatry and behavioral neuroscience at the University of Chicago who led several of the studies. “We see brain changes that are a little bit like the high dose effect,” which suggests the smaller doses are acting on the same systems.Some microdosing researchers, like Dr. de Wit and Dr. van Elk, remain optimistic that tiny amounts of hallucinogenic drugs will ultimately prove beneficial for mental health and cognition. They say that the design of the placebo-controlled trials may be to blame for their lack of significant findings. The studies may not have run for long enough, or the tests and questionnaires used during the studies may not fully capture the benefits some people experience from microdosing.On the other side, Dr. Erritzoe said that just because a drug has an impact on the brain doesn’t mean it has any therapeutic value. “If you can’t see in a proper trial that it works for the symptoms, for things that people can actually detect and feel and experience in their lives, then it’s just not that interesting,” he said.“I’m not trying to shoot down microdosing,” he added. “I’m just being cautious and saying at the moment, it does not look particularly optimistic.”One of the biggest problems with microdosing research is that it’s hard to block the placebo effect in studies of a psychoactive substance. In Dr. Erritzoe’s trial, 72 percent of people correctly guessed what they had taken, which means it’s no longer blinded. For the studies showing effects in the brain, the biggest changes came at the higher end of the microdosing spectrum — 20 to 26 micrograms of LSD and 3 milligrams of psilocybin — an amount where people often start noticing the drug’s effects.Out of the lab, most users dose themselves aiming for a similar subtle awareness that they’ve taken something. At that level, the microdose might be closer to a half dose, or their expectations could heighten the drug’s benefits because they can feel that it’s doing something.As a result of these difficulties and the lack of conclusive findings, Dr. van Elk has abandoned microdosing research to go back to studying large doses of the drugs. Dr. Erritzoe said once his next study ends, he’ll probably do the same.Both Joseph and Ms. Royal are aware that the benefits of microdosing could be a placebo effect. But for them, how it works matters less than the fact that it’s helped. These days, Joseph said his depression has improved thanks to a regular meditation practice, although he still microdoses occasionally if he starts feeling down.After several years of microdosing, he said the biggest change he’s experienced is a general shift in his mind set — something that’s harder for scientists to measure. “I started because I read that it helps with depression,” he said. “But as I’ve moved on, it’s helped really a lot more with mental and personal growth and outlook on life — how you want to live and your existence in the world.”Dana Smith is an award-winning health and science writer based in Durham, North Carolina. Her work has appeared in The Atlantic, The Guardian, Scientific American, Popular Science and more.

People who are more physically fit are less likely to develop Alzheimer’s disease than people who are less physically fit, according to a preliminary study released today, February 27, 2022, that will be presented at the American Academy of Neurology’s 74th Annual Meeting being held in person in Seattle, April 2 to 7, 2022 and virtually, April 24 to 26, 2022.
“One exciting finding of this study is that as people’s fitness improved, their risk of Alzheimer’s disease decreased — it was not an all-or-nothing proposition,” said study author Edward Zamrini, MD, of the Washington VA Medical Center in Washington, D.C., and a member of the American Academy of Neurology. “So people can work toward making incremental changes and improvements in their physical fitness and hopefully that will be associated with a related decrease in their risk of Alzheimer’s years later.”
The study involved 649,605 military veterans in the Veterans Health Administration database with an average age of 61 who were followed for an average of nine years. They did not have Alzheimer’s disease at the start of the study.
Researchers determined participants’ cardiorespiratory fitness. Cardiorespiratory fitness is a measure of how well your body transports oxygen to your muscles, and how well your muscles are able to absorb oxygen during exercise.
The participants were divided into five groups, from least fit to most fit. Fitness levels were determined by how well participants did on a treadmill test. This test measures exercise capacity, the highest amount of physical exertion a person can sustain. For people who are middle-aged and older, the highest level of fitness can be achieved by walking briskly most days of the week, for two and a half hours or more per week.
The group with the lowest level of fitness developed Alzheimer’s at a rate of 9.5 cases per 1,000 person-years, compared to 6.4 cases per 1,000 person-years for the most fit group. Person-years take into account the number of people in a study as well as the amount of time spent in the study. The case rate decreased as the level of fitness increased, with a rate of 8.5 for the second least fit group, 7.4 for the middle group and 7.2 for the second most fit group.
When researchers adjusted for other factors that could affect risk of Alzheimer’s disease, they found that the people in the most fit group were 33% less likely to develop Alzheimer’s disease than those in the least fit group. The second most fit group was 26% less likely to develop the disease, while the middle group was 20% less likely and those in the second least fit group were 13% less likely to develop the disease than those in the least fit group.
“The idea that you can reduce your risk for Alzheimer’s disease by simply increasing your activity is very promising, especially since there are no adequate treatments to prevent or stop the progression of the disease,” Zamrini said. “We hope to develop a simple scale that can be individualized so people can see the benefits that even incremental improvements in fitness can deliver.”
A limitation of the study was participants were mostly white men so results may not be generalizable to other populations.
The study was supported by the National Institute on Aging, the National Institutes of Health, the U.S. Department of Veterans Affairs, the Washington D.C. VA Medical Center and George Washington University.
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The innate immune system plays a crucial role in regulating host-microbe interactions, and especially in providing protection against pathogens that invade the mucosa. Using an intestinal infection model, scientists from the Institut Pasteur and Inserm discovered that innate effector cells — group 3 innate lymphoid cells — act not only during the early stages of infection but can also be trained to develop an innate form of immunological memory that can protect the host during reinfection. The study was published in the journal Science on February 25, 2022.
Combating Escherichia coli infections, which are responsible for intestinal diseases or gastrointestinal bleeding, is a major public health challenge. These bacteria, which are present in drinking water or food, can cause persistent diarrhea associated with acute intestinal inflammation. Consequently, enteropathogenic and enterohemorrhagic Escherichia coli are responsible for nearly 9% of child deaths worldwide.
The gut mucosa harbors a complex defense system that allows it to combat pathogen infection while maintaining tolerance to commensal microbiota, which are essential for the normal bodily function. This constant surveillance is performed by the innate immune system, which provides early defense in the initial hours after infection. The adaptive immune system then develops a memory for the pathogens that it encounters by activating specific receptors expressed at the surface of B and T lymphocytes, thereby enabling the production of protective antibodies and inflammatory cytokines. Unlike the clearly established function of the adaptive system in long-term tolerance and protection, the role of the innate system in immune memory remains to be determined.
In 2008, the team led by Inserm scientist James Di Santo (Innate Immunity Unit, Institut Pasteur/Inserm) described group 3 innate lymphoid cells (ILC3s) as a novel family of lymphocytes that were distinct from adaptive T and B lymphocytes. ILC3s play an essential role in the innate immune response, especially in the gut mucosa, by producing pro-inflammatory cytokines, such as interleukin (IL)-22. The cytokine release activates the production of antimicrobial peptides by epithelial cells, thereby reducing the bacterial load in order to maintain the integrity of the intestinal barrier.
In this study, scientists from the Innate Immunity Unit (Institut Pasteur/Inserm) used an innovative protocol to expose the immune system to a time-restricted enterobacterial challenge based on Citrobacter rodentium (a mouse model of E. coli infection). They observed that ILC3s persist for several months in an activated state after exposure to C. rodentium. During a second infection, the “trained” ILC3s have a superior capacity to control infection through an enhanced proliferation and massive production of IL-22. “Our research demonstrates that intestinal ILC3s acquire a memory to strengthen gut mucosal defenses against repeated infections over time,” explains Nicolas Serafini, first author of the study and an Inserm scientist in the Innate Immunity Unit (Institut Pasteur/Inserm).
“The ability to “train” the innate immune system in the mucosa paves the way for improvements to the body’s defenses against a variety of pathogens that cause human diseases,” comments James Di Santo, last author of the study and Head of the Innate Immunity Unit (Institut Pasteur/Inserm).
This discovery demonstrates a new antibacterial immune defense mechanism and could lead, in the long term, to novel therapeutic approaches to treat intestinal diseases (IBD or cancer).
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