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Research and Press Releases

Novel Immune Cell Population May Trigger Inflammation in Multiple Sclerosis and other Brain Disorders

A group of immune cells that normally protect against inflammation in the gastrointestinal tract may have the opposite effect in multiple sclerosis (MS) and other brain inflammation-related conditions, according to a new study by Weill Cornell Medicine and NewYork-Presbyterian researchers. The results suggest that countering the activity of these cells could be a new therapeutic approach for such conditions.

The researchers, who reported their finding Dec. 1 in Nature, were studying a set of immune cells called group 3 innate lymphoid cells (ILC3s), which help the immune system tolerate beneficial microbes and suppress inflammation in the intestines and other organs throughout the body. They discovered a unique subset of these ILC3s that circulate in the bloodstream and can infiltrate the brain—and, to their surprise, do not quench inflammation but instead ignite it.

The scientists called this subset inflammatory ILC3s, and found them in the central nervous system of mice with a condition modeling MS. Instead of constraining the immune response, this subset of ILC3s spurred another group of immune cells called T cells to attack myelinated nerve fibers, leading to MS-like disease symptoms. The researchers detected similar inflammatory ILC3s in the peripheral blood and cerebrospinal fluid of MS patients.

“This work has the potential to inform our understanding of, and potential treatments for, a broad variety of conditions involving T-cell infiltration of the brain,” said senior author Dr. Gregory Sonnenberg, associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine.

Dr. Greg Sonnenberg and John Benji Grigg

Dr. Greg Sonnenberg (left) and John Benji Grigg

MS affects more than two million people worldwide. Other conditions that feature chronic brain inflammation afflict tens of millions more and include Alzheimer’s and Parkinson’s diseases. There is also evidence that neuroinflammation develops naturally with aging and is a major factor in age-related cognitive decline, and more recently inflammatory T-cell responses in the brain have been linked to neurological symptoms associated with SARS-CoV-2 infection.

The researchers have shown in recent work that ILC3s residing in the gut act as sentinels and immune regulators, suppressing inflammation—including inflammatory T-cell activity—and warding off cancer. In the new study, they examined the roles of ILC3s in the brain, and found, contrary to their expectation, that ILC3s are not normally present in the brain under healthy conditions but can infiltrate the brain from the bloodstream during inflammation. When they do infiltrate the central nervous system, they have pro-inflammatory rather than anti-inflammatory effects.

The researchers showed with a mouse model of MS that these inflammatory ILC3s in the brain function as antigen-presenting cells: They display bits of myelin protein, the main ingredient in the insulating layer around nerve fibers, to T cells—prompting them to attack myelin, causing the nerve damage that gives rise to disease signs. They found the inflammatory ILC3s in close association with T cells in regions of active inflammation and nerve damage in the mouse brains. To read more, click here.


Antibodies Help Keep Harmful Forms of Gut Fungi in Check

Antibody protection against harmful forms of fungi in the gut may be disrupted in some patients with Crohn’s disease—a condition caused by chronic inflammation in the bowel—according to a new study by Weill Cornell Medicine investigators.

Previous studies have shown that the immune system plays a key role in maintaining a healthy balance of gut bacteria. In the new study, published Nov. 22 in Nature Microbiology, senior author Dr. Iliyan Iliev, associate professor of immunology in medicine in the Division of Gastroenterology and Hepatology, and his team at Weill Cornell Medicine investigated if it might also play a role in managing gut fungi. Unlike bacteria, fungi can change their shape in response to environmental conditions, and certain forms are harmful to humans. In particular, a type of fungus called Candida albicans transforms from a yeast form that is not pathogenic to a form that produces long, branched structures called hyphae, which can invade tissues and cause damage.

two men posing for a photo

(From left) Dr. Iliyan Iliev and Itai Doron.

The investigators found that antibodies that are secreted in the gut help control the pathogenesis of Candida albicans in healthy individuals and that this protective mechanism may be disabled in people with Crohn’s disease, causing a harmful overgrowth of the pathogenic form of the fungus. An intestinal overabundance of Candida albicans is associated with inflammatory bowel disease and several other conditions that directly or indirectly affect the gastrointestinal tract.

“We found that antibodies secreted in the gut are involved in maintaining specific intestinal fungi such as C. albicans in its benign, so-called commensal form,” said Dr. Iliev, who is also a scientist in the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. “This process is interrupted in patients with Crohn’s disease.” To read more, click here.


Researchers Identify Bacteria That Underlie Success of Fecal Microbiota Transplants

Circular genome map of Odoribacter splanchnicus isolated from an ulcerative colitis patient. Image courtesy of Drs. Longman and Lima.

The effectiveness of fecal microbiota transplantation (FMT) in treating ulcerative colitis depends on a small set of beneficial bacterial strains, suggests a new study from researchers at Weill Cornell Medicine and NewYork-Presbyterian.

In the study, reported Oct. 1 in Gastroenterology, the researchers sampled gut bacteria from healthy FMT donors and from FMT recipients with ulcerative colitis, identifying the bacterial strains whose transfer correlates with treatment effectiveness.

The scientists found that one of these strains was linked particularly strongly to treatment success. They showed that its protection against colitis involves several interrelated mechanisms, including the induction of an increase in anti-inflammatory T cells in the gut, and the production of anti-inflammatory, gut health-promoting molecules called short-chain fatty acids.

“Fecal microbiota transplant has been shown to be effective in several clinical trials, but ultimately we need to identify the specific microbial factors that make it work and focus on delivering those,” said senior author Dr. Randy Longman, director of the Jill Roberts Center for Inflammatory Bowel Disease at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center. “This study takes us a significant step closer to that goal.”

Scientists over the past two decades have begun to recognize the broad importance of gut-resident bacteria in regulating human health, especially immune system and gut health. Both of these are disrupted in ulcerative colitis, the most common form of inflammatory bowel disease, which affects more than two million people worldwide. To read more, click here.


Key Immune Cells Maintain Healthy Gut Bacteria to Protect Against Colorectal Cancer

Artistic rendering of a tumor growing within a colon, resulting in local alterations of resident microbiota. Artist/Image Source: Sarah Field Sonnenberg

An immune cell subset called innate lymphoid cells (ILC3s) protects against colorectal cancer, in part by helping to maintain a healthy dialogue between the immune system and gut microbes, according to a new study led by researchers at Weill Cornell Medicine and NewYork-Presbyterian. The finding opens the door to new strategies for treating this type of cancer.

The researchers, who published their findings August 17 in Cell, showed that ILC3s tend to be drastically reduced and functionally altered in people with colorectal cancer. Further, they demonstrate that experimentally disrupting the functions of ILC3s in mice leads to aggressive colon cancer and greatly reduces the effectiveness of cancer immunotherapies.

Colorectal cancer is the fourth most common cancer in the United States, with about 150,000 new cases each year and about 50,000 deaths. While early detection of these cancers or precancerous polyps with screening colonoscopies is very effective, treatments for advanced colorectal tumors remain a major challenge with limited therapeutic options. Oncologists are particularly concerned about the relative resistance of these tumors to immunotherapies—treatments that work well against some other cancers by boosting the immune system’s ability to attack malignant cells.

Dr. Greg Sonnenberg

Dr. Greg Sonnenberg

“These findings suggest new possibilities for the clinical approach to colorectal cancer, and also help explain why this type of cancer often fails to respond to immunotherapies,” said senior author Dr. Gregory Sonnenberg, an associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine.

One factor impacting the resistance to immunotherapies may be the gut microbiome, the population of bacteria and other microbial species that reside in the intestines and normally aid digestion, support various metabolic functions and play a role in regulating the immune system. Colorectal cancer is associated with chronic gut inflammation and a major disruption of the normal microbiome. Further, recent studies suggest that patients’ microbiomes play a key role in controlling the outcome of cancer immunotherapies and may explain why some patients’ cancers do, or do not, respond well to treatment.

In the new study, Dr. Sonnenberg and colleagues, including lead author Dr. Jeremy Goc, a research associate in Dr. Sonnenberg’s laboratory, examined the role of ILC3s, which reside in the intestines and are known to help mediate the relationship between the immune system and gut microbes.

Among this loss of normal ILC3 activity in the gut, the authors further observed that the ability of ILC3s to regulate a specific immune cell subset called T cells was significantly disrupted. This disruption of the dialogue between ILC3s and T cells further led to a rise in inflammation in the gut that subsequently modifies the gut microbiome. These gut microbe changes in turn induce a decrease in the levels of T cells that are good at fighting tumors.

Dr. Jeremy Goc

Group 3 innate lymphoid cells normally play a key role in maintaining a healthy dialogue between the microbiome and the immune environment in the lower gut. In close collaboration with Dr. Manish Shah, the Bartlett Family Professor of Gastrointestinal Oncology director of the Gastrointestinal Oncology Program in the Division of Hematology and Medical Oncology, and member of the Sandra and Edward Meyer Cancer Center at Weill Cornell Medicine, the research group analyzed colorectal tumors and pre-cancerous polyps from humans and mice. They found that ILC3s from cancerous tissues were relatively depleted as compared with healthy tissues and were further fundamentally altered in their functions.

“This is an exciting finding that could have broad implications for our understanding of the pathways that control the pathogenesis, progression and therapeutic responsiveness of gastrointestinal malignancies,” said study co-author Dr. Shah, who is also chief of the Solid Tumor Oncology Service and co-director of the Center for Advanced Digestive Care at NewYork-Presbyterian/Weill Cornell Medical Center.

Among this loss of normal ILC3 activity in the gut, the authors further observed that the ability of ILC3s to regulate a specific immune cell subset called T cells was significantly disrupted. This disruption of the dialogue between ILC3s and T cells further led to a rise in inflammation in the gut that subsequently modifies the gut microbiome. These gut microbe changes in turn induce a decrease in the levels of T cells that are good at fighting tumors. To read more, click here.


Study Identifies ‘Achilles heel’ of Bacteria Linked to Crohn’s Disease

The discovery of an “Achilles heel” in a type of gut bacteria that causes intestinal inflammation in patients with Crohn’s disease may lead to more targeted therapies for the difficult to treat disease, according to Weill Cornell Medicine and NewYork-Presbyterian investigators.

In a study published Feb. 3 in Cell Host and Microbe, the investigators showed that patients with Crohn’s disease have an overabundance of a type of gut bacteria called adherent-invasive Escherichia coli (AIEC), which promotes inflammation in the intestine. Their experiments revealed that a metabolite produced by the bacteria interacts with immune system cells in the lining of the intestine, triggering inflammation. Interfering with this process, by either reducing the bacteria’s food supply or eliminating a key enzyme in the process relieved gut inflammation in a mouse model of Crohn’s disease.

“The study reveals a therapeutically targetable weak point in the bacteria,” said senior author Dr. Randy Longman, associate professor of medicine in the Division of Gastroenterology and Hepatology and the Director of the Jill Roberts Center for Inflammatory Bowel Disease at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center.

a woman smiling for a photo

Dr. Monica Viladomiu

To find this “Achilles heel,” Dr. Longman and his colleagues, including Drs. Ellen Scherl and Chun-Jun Guo at Weill Cornell Medicine and collaborators Dr. Gretchen Diehl at Memorial Sloan Kettering and Dr. Kenneth Simpson at Cornell’s Ithaca campus, targeted a process the AIEC bacteria uses to convert a byproduct of sugar fermentation in the gut to grow. Specifically, the AIEC uses 1,2-propanediol, a byproduct of the breakdown of a type of sugar called fucose that is found in the lining of the intestines. When the AIEC converts 1,2-propanediol, it produces propionate, which the study showed interacts with a type of immune system cell called mononuclear phagocytes that are also found in the lining of the gut. This sets off a cascade of inflammation.

Next, the investigators genetically engineered AIEC bacteria to lack a key enzyme in this process called propanediol dehydratase. Without propanediol dehydratase, the bacteria do not set off a cascade of inflammation in a mouse model of Crohn’s disease. Reducing the available supply of fucose in the animal’s gut also reduced inflammation.

“Changing one metabolic pathway in one type of bacteria can have a big impact on intestinal inflammation,” said the study’s co-lead author Dr. Monica Viladomiu, a post-doctoral associate in medicine in the Division of Gastroenterology and Hepatology and in the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. Maeva Metz, a Weill Cornell Medicine Graduate School of Medical Sciences doctoral candidate in Dr. Longman’s laboratory, is also co-lead author.

a woman smiling for a photo

Maeva Metz

The discovery could lead to better treatments for Crohn’s disease, a type of inflammatory bowel disease that affects more than 4 million people worldwide. Currently, patients with Crohn’s disease are often treated with antibiotics, which can kill both beneficial and harmful bacteria causing unwanted side effects. But treatments that precisely target the inflammatory cascade discovered by Dr. Longman and colleagues might help reduce inflammation while preserving beneficial bacteria.

“If we can develop small molecule drugs that inhibit propanediol dehydratase or use dietary modifications to reduce the availability of fucose, we may be able to reduce intestinal inflammation in patients with Crohn’s disease with fewer side effects,” said Dr. Longman, who is also a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease.

One of the next steps for the team will be testing potential treatments. They also plan to study the potential role of an enzyme called fucosyltransferase 2 in protecting the gut against this inflammatory cascade. Dr. Longman explained that many patients with Crohn’s disease have mutations in the gene that encodes this enzyme, rendering it nonfunctional.

“From a clinical perspective, that's interesting because it may help us stratify people for whom one intervention or another maybe more useful,” Dr. Longman said.


Fungi in the Gut Prime Immunity Against Infection


Weill Cornell Medicine Scientist Receives Pathogenesis of Infectious Disease Award

Dr. Iliyan Iliev, an associate professor of immunology in medicine in the Division of Gastroenterology and Hepatology and a scientist in the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine, has been awarded the Investigators in the Pathogenesis of Infectious Disease (PATH) award by the Burroughs Wellcome Fund.

The PATH award provides early-career scientists with $500,000 over five years to investigate the interplay between humans and pathogens, and how such encounters can lead to disease. These prestigious awards are intended to give the freedom and flexibility to pursue new avenues of inquiry, stimulating higher risk research projects that hold potential for significantly advancing understanding of how infectious diseases work and how health is maintained.

“This award is not only a great recognition, but it’s also a trust that the Burroughs Wellcome Fund has in us to go in a direction that we haven’t yet explored in our lab,” Dr. Iliev said.

The PATH award will allow Dr. Iliev to explore processes that allow fungi to breach intestinal barriers and cause systemic Candidiasis, which is the most common type of systemic fungal infection caused by a yeast called Candida albicans that is found in humans. To read more, click here.


Dr. Gregory Sonnenberg Awarded The 2020 ICIS-Luminex John R. Kettman Award For Excellence in Interferon & Cytokine Research

Above left: Lymphoid Follicle in the colon of a healthy mouse demonstrating the presence of RORgt+ILC3. The section is stained for RORgt (green), IL-7Ra (red) and CD3 (blue). Image courtesy of Dr. Gregory Sonnenberg

The Jill Roberts Institute for Research in IBD is pleased to announce that one of our esteemed faculty members, Dr. Gregory Sonnenberg, an associate professor of microbiology and immunology in medicine, was awarded the inaugural ICIS-LUMINEX John R. Kettman Award for Excellence in Interferon & Cytokine Research from the international Cytokine & Interferon Society. The award recognizes mid-level investigators who have made outstanding contributions to the field of interferon or cytokine biology. Dr. Sonnenberg was honored for his scientific contributions to the fields of immunology and microbiology, and for his success as an independent, extramurally funded investigator. To read more about Dr. Sonnenberg and other Weill Cornell Medicine awards and honors that were bestowed in October 2020, please click here.


Dr. Sonnenberg Receives ICIS-LUMINEX John R. Kettman Award for Excellence in Interferon & Cytokine Research

sonnenberg-gregory

Dr. Gregory F. Sonnenberg, Associate Professor of Microbiology & Immunology in Medicine, Division of Gastroenterology and Hepatology, WDOM, has received the inaugural ICIS-LUMINEX John R. Kettman Award for Excellence in Interferon & Cytokine Research.

The ICIS-LUMINEX John R. Kettman Award for Excellence in Interferon & Cytokine Research recognizes Dr. Sonnenberg for “establishing himself as an extramurally funded and well-respected independent investigator, and his innovative research program which continues to make seminal scientific contributions at the interface of immunology and microbiology.”

The WDOM congratulates Dr. Sonnenberg on receiving this prestigious award.


COVID-19 Research Grants Support Weill Cornell Medicine Investigators

Weill Cornell Medicine has awarded eight grants of $100,00 each to faculty for a variety of research projects on COVID-19, funded by the institution’s Board of Overseers and additional donors. The grants will support studies aimed at understanding fundamental aspects of the disease, the body’s immune response and social determinants of health that affect COVID-19 outcomes.

One of the faculty members selected as a grant recipient is Julie Magarian Blander, Ph.D., the Gladys and Roland Harriman Professor of Immunology in Medicine, who is also a faculty member of the Jill Roberts Institute for IBD. Immunologists are uniquely poised to make an impact and contribution through their investigation into COVID-19 that may have a global effect on the pandemic. Dr. Blander’s research project, A T cell Biomarker for Protective COVID-19 Immunity, is summarized in following paragraph.

Identifying patients who have recovered from COVID-19 and are immune to future infection is essential to emerging from the pandemic. To do this, scientists must develop reliable tests for immunity to the SARS-CoV-2 virus. Though testing for antibodies to the virus is common, so far it is unclear whether they protect against future infection. Dr. Blander and her team will use blood collected from Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center healthcare workers who recovered from COVID-19 to find virus-fighting immune cells called CD8 T cells. They will then identify the receptor these T cells use to find and destroy cells infected with the SARS-CoV-2 virus and try to develop a test to determine if individuals with this receptor are safe from future infections. If they are successful, it could lead to new tests that identify people who are protected from COVID-19 because they have recovered from SARS-CoV-2 infection or from a previous infection with a similar virus that generates a similar immune response.

 

To read the full WCM article about all eight grant recipients, please follow the link here.


Fungus in Gut May Explain Why Some Ulcerative Colitis Patients Benefit from Fecal Transplant

Higher levels of a type of fungus in the gut are associated with better outcomes for patients with a type of inflammatory bowel disease called ulcerative colitis who are treated with gut microbes from healthy donors, according to a new study by Weill Cornell Medicine investigators.

The study, published April 15 in Cell Host & Microbe, suggests a way to determine which patients may be good candidates for the therapy, called fecal microbiota transplant (FMT), in which stool—and the healthy bacteria, fungi and other microbes it contains—are transferred from a donor to the patient.

Ulcerative colitis is a type of inflammatory bowel disease that causes chronic sores and inflammation in the colon and rectum. Prior research has shown that FMT can promote healing in the mucosal lining of the lower digestive tract, relieving ulcerative colitis symptoms in some people. Based on the new study, those patients who benefit from this therapy have higher levels of the fungus Candida in their gut prior to the procedure.

Graphic depicting association of Candida levels with response to fecal microbiota transplant in ulcerative colitis patients.

“The fecal transplant then acts to decrease the population of Candida,” said senior study author Dr. Iliyan D. Iliev, assistant professor of immunology in medicine in the Division of Gastroenterology and Hepatology and co-director of the Microbiome Core Lab at the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. While more research is needed, the decline in Candida after FMT may help to reduce inflammation in the colon and rectum. “Altered fungus levels may also affect bacteria in the gut, altogether reducing inflammation,” said Dr. Irina Leonardi, first author of the study and a postdoctoral associate in medicine at Weill Cornell Medicine.

About 750,000 people in North America have ulcerative colitis. The disease does not always respond to medication, and while surgery can relieve symptoms, it is not curative. The current research may one day help doctors determine which patients might be candidates for FMT or other microbiome-based therapies. To read more, click here.


Scientists Identify New Pathways to Inflammation in Allergy-Linked Immune Cells

The protein interleukin-33 (shown in green) in the cell nucleus (blue) of stromal cells (red) of mucosal tissue that is embedded in visceral adipose tissue (large octagonal purple cells). Image courtesy of Dr. Tanel Mahlakõiv and Dr. David Artis, WCM.

A class of immune cells push themselves into an inflammatory state by producing large quantities of a serotonin-making enzyme, according to a study in mice led by scientists at Weill Cornell Medicine.

The study, published March 10 in Immunity, found that the inflammatory and infection-fighting abilities of the cells, called type 2 innate lymphoid cells (ILC2s), are much impaired without the enzyme. The finding suggests possibilities for new treatments targeting ILC2s, which have been linked to asthma and other allergic disorders, to suppress their activation in inflammatory disorders.

The work also hints at what could be a major mechanism of “cross-talk” between the nervous system, which uses serotonin as a signaling molecule or neurotransmitter, and the immune system.

“There’s a lot more to do in terms of understanding the biology of these innate lymphoid cells, but it’s an exciting area that offers us potential new approaches to therapeutic intervention,” said study senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease, director of the Friedman Center for Nutrition and Inflammation and the Michael Kors Professor of Immunology in the Department of Medicine at Weill Cornell Medicine.

Innate lymphoid cells are a recently discovered family of white blood cells that reside in the skin, airways and other barrier tissues of the body. They appear to have important roles as first-responders against environmental pathogens, but scientists also recognize that ILCs may hold the keys to understanding common inflammatory and autoimmune conditions such as asthma and inflammatory bowel disease. To read more, click here.


Immune Cells Heal the Intestine by Controlling Iron

An iron-regulating molecule called hepcidin is produced by the immune system and restricts the growth of gut bacteria after an intestinal injury, helping to heal the lining of the intestine, according to a study by Weill Cornell Medicine, NewYork-Presbyterian and Institut Cochin investigators.

The study, published April 10 in Science, was conducted in mice and human samples and could have important implications for treating gastrointestinal diseases that damage the lining of the intestines as a result of infection, chronic inflammation or cancer. Currently, most treatments for gut-damaging conditions like inflammatory bowel disease (IBD) focus solely on reducing inflammation and do not directly address the need to promote tissue repair.

“Not being able to heal your intestine is a major problem in patients with inflammatory bowel disease and other gastrointestinal disorders,” said senior author Dr. Gregory F. Sonnenberg, associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. “There is an urgent need to better understand the pathways that promote mucosal healing and harness that knowledge to design new treatment strategies.”

Bleeding in the intestines is often one the first signs of diseases like IBD or colorectal cancer, said lead author Dr. Nicholas Bessman, a postdoctoral associate in medicine at Weill Cornell Medicine. Intestinal bleeding may further exacerbate these diseases or hamper healing by fueling overgrowth of gut bacteria. This happens because blood contains large amounts of iron, which is essential for bacterial growth. To investigate the potential role of the iron-regulator hepcidin, the team collaborated with Dr. Carole Peyssonnaux and other researchers at the Université de Paris, INSERM, Institut Cochin, and examined intestinal healing in mice with and without the hepcidin gene. To read further, please click here.

From left: Drs. Robbyn Sockolow and Gregory Sonnenberg

Dr. Nicholas J. Bessman


New Technique Allows Genome Editing of Gut Bacteria

Scientists at Weill Cornell Medicine, Stanford University and the University of California, San Francisco have adapted genome editing tools to function in a common species of intestinal bacteria. With this technological advance, they can now precisely alter the human gut microbes’ production of small molecule metabolites that can affect their host’s metabolism, immune system and nervous system. The technique has revealed a new regulator of mucosal immune function, which operates at the externally facing surfaces that line organs such as the gut and the lungs. It could also form the basis for genetically engineering the gut microbiota to promote human health or treat disease.

Humans and other animals host thriving populations of microbes on and in their bodies. In recent years, investigators have found that these bacteria, viruses and fungi, collectively called the microbiota, exert profound influence on their hosts’ metabolism and disease pathology. The intestinal microbiota are especially diverse, varying from one individual to the next and hosting microbes that produce thousands of small molecules.

“There are many studies addressing associations between the gut microbiota and human diseases,” said Dr. Chun-Jun Guo, an assistant professor of immunology in medicine in the Division of Gastroenterology and Hepatology at Weill Cornell Medicine and lead author on the new study, published Dec. 13 in Science. Because the gut microbes appear to exert their influence on the host through the various bacterial metabolites they excrete, Dr. Guo and his colleagues wanted to probe these phenomena more thoroughly and understand the underlying mechanisms. “We wanted to develop a technology that allows us to manipulate the level of these bacterial metabolites or genes in vivo so we can directly study their impacts on the host biology,” Dr. Guo said. To read more, click here.


CURE For IBD presents donation in continuing partnership with Jill Roberts Institute

Photo above: From left to right, Front row: Kassi Reicin, Kyla Reicin, Lina Krivyan, Dr. Robbyn Sockolow, Benjamin Goldmark, Patti Kaufman, Dr. Ellen Scherl, and Jill Roberts From left to right, Back row: Joe Lepler, Chris Pedicone, Dr. David Artis, Thomas Plaza, Dr. Tom Haverty

Photo below: From left to right, Front row: Dr. Robbyn Sockolow, Benjamin Goldmark, Patti Kaufman and Dr. Ellen Scherl From left to right, Back row: Dr. David Artis, Chris Pedicone, Thomas Plaza, Elizabeth Goldmark

Since 2017, the Jill Roberts Institute for Research in Inflammatory Bowel Disease (IBD) and its Director, Dr. David Artis, have partnered with Chris Pedicone, Founder and President of CURE for IBD for a fruitful collaboration between laboratory research and dedicated fundraising efforts to find a cure for inflammatory bowel disease. CURE for IBD is a volunteer non-profit organization devoted solely to funding IBD research that seeks new treatments and cures for family, friends, and others living with IBD. On February 14, 2020, the CURE for IBD team, including Benjamin Goldmark, Elizabeth Goldmark, Dr. Tom Haverty, Patti Kaufman, Lina Krivyan, Joe Lepler, Chris Pedicone, Thomas Plaza, Kassi Reicin, and Kyla Reicin, visited the Jill Roberts Institute for discussion and a tour of the laboratory facilities. At the close of their visit, CURE for IBD graciously presented the Jill Roberts Institute with a check for $50,000 to support IBD research efforts. This year included a special $2,000 donation from Benjamin Goldmark, who chose to raise funds for CURE for IBD to complete his Bar Mitzvah project and to honor a family member who lives with IBD. Dr. Artis and members of the Jill Roberts Institute extend their gratitude to CURE for IBD and celebrate this ongoing partnership that supports current and future IBD research efforts.


Gut Instincts: Researchers Discover First Clues on How Gut Health Influences Brain Health

New cellular and molecular processes underlying communication between gut microbes and brain cells have been described for the first time by scientists at Weill Cornell Medicine and Cornell’s Ithaca campus.

Over the last two decades, scientists have observed a clear link between autoimmune disorders and a variety of psychiatric conditions. For example, people with autoimmune disorders such as inflammatory bowel disease (IBD), psoriasis and multiple sclerosis may also have depleted gut microbiota and experience anxiety, depression and mood disorders. Genetic risks for autoimmune disorders and psychiatric disorders also appear to be closely related. But precisely how gut health affects brain health has been unknown.

“Our study provides new insight into the mechanisms of how the gut and brain communicate at the molecular level,” said co-senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease, director of the Friedman Center for Nutrition and Inflammation and the Michael Kors Professor of Immunology at Weill Cornell Medicine. “No one yet has understood how IBD and other chronic gastrointestinal conditions influence behavior and mental health. Our study is the beginning of a new way to understand the whole picture.”

For the study, published Oct. 23 in Nature, the researchers used mouse models to learn about the changes that occur in brain cells when gut microbiota are depleted. First author Dr. Coco Chu, a postdoctoral associate in the Jill Roberts Institute for Research in Inflammatory Bowel Disease, led a multidisciplinary team of investigators from several departments across Weill Cornell Medicine, Cornell’s Ithaca campus, the Boyce Thompson Institute, Broad Institute at MIT and Harvard, and Northwell Health with specialized expertise in behavior, advanced gene sequencing techniques and the analysis of small molecules within cells.

Mice treated with antibiotics to reduce their microbial populations, or that were bred to be germ-free, showed a significantly reduced ability to learn that a threatening danger was no longer present. To understand the molecular basis of this result, the scientists sequenced RNA in immune cells called microglia that reside in the brain and discovered that altered gene expression in these cells plays a role in remodeling how brain cells connect during learning processes. These changes were not found in microglia of healthy mice. To read more, click here.


It’s all about timing—JRI Researchers identify an essential role for the circadian clock in regulating innate lymphoid cell homeostasis in the gut

Regular daily changes between light and dark has enormous impacts on behavior and physiology of humans and many other mammals (also known as circadian rhythm). Disturbance of normal circadian rhythm in humans by shifted work, sleep disorders or frequent inter-continental flights is causally associated with obesity, cardiovascular diseases and intestinal disorders such as irritable bowel syndrome or inflammatory bowel disease. In a new study published on Oct. 4th, 2019 in Science Immunology and highlighted by the journal cover image, researchers from Weill Cornell Medicine have identified that the homeostasis of group 3 innate lymphoid cells (ILC3s), one of the key immune cell populations regulating intestinal immunity and barrier function, critically requires circadian rhythm.

 

The study was led by Dr. Gregory Sonnenberg, an associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine, and Dr. Fei Teng, a postdoctoral researcher in the Sonnenberg Lab. The researchers found that intestinal ILC3s in mice exhibit diurnal oscillations in genes involved in both circadian clock and classical ILC3 effector functions in response to light signals. By genetic ablation of this pathway, they also found circadian regulation is essential for survival and appropriate cytokine production of ILC3s in the presence of intestinal commensal bacteria. Lastly, the researchers identified ILC3s isolated from the inflamed intestine of patients with inflammatory bowel disease exhibited substantial alterations in expression of several circadian-related genes. This study has uncovered a previously under-appreciated role of circadian rhythm on the homeostasis of intestinal ILC3s and suggested that this pathway may serve as a novel target to boost or restore normal ILC3 responses in the context of intestinal inflammation.

 

This work is in collaboration with Dr. Manish A. Shah (NewYork-Presbyterian Hospital) and Dr. Gérard Eberl (Institut Pasteur, France) and was supported by the NIH (R01AI143842, R01AI123368, R01AI145989, and U01AI095608), the NIAID Mucosal Immunology Studies Team (MIST), the Crohn’s and Colitis Foundation of America, the Searle Scholars Program, the American Asthma Foundation Scholar Award, Pilot Project Funding from the Center for Advanced Digestive Care (CADC), an Investigators in the Pathogenesis of Infectious Disease Award from the Burroughs Wellcome Fund, a Wade F.B. Thompson/Cancer Research Institute CLIP Investigator grant, the Cancer Research Institute Lloyd J. Old STAR Program, the Meyer Cancer Center Collaborative Research Initiative, and the Jill Roberts Institute (JRI) for Research in IBD.


2019 NYC IBD Day Held at Weill Cornell Medicine

Image Credits: Jennifer Conrad

On September 18, 2019, the 5th Annual New York City IBD Research Day was hosted by Weill Cornell Medicine in the Belfer Research Building. This yearly symposium is a collaborative effort of five institutions: The Jill Roberts Institute at Weill Cornell Medicine, The Immunology Institute of the Icahn School of Medicine at Mount Sinai, The Center for Basic and Translational Research on Disorders of the Digestive System at The Rockefeller University and The Skirball Institute and the Departments of Medicine and Surgery at New York University Langone Health and Columbia University, who joined the group last year. In honor of the late Lloyd F. Mayer, MD, there is a Mayer Prize given yearly. Drs. Sergio Lira and David Artis presented the Mayer Prize to their colleague, Dr. Yasmine Belkaid. Dr. Belkaid, highly esteemed for her research examining the microbiota’s ability to build a immunological response to infection in the GI tract and skin, started the day with her talk on “Regulation of Tissue Inflammation.” Dr. Belkaid also received the Lurie Prize in Biomedical Sciences in 2019 for her outstanding achievements in biomedical research. Throughout the course of the day, the attendees listened to ten presenters, who had traveled from around the globe for this event, engaging in lively Q & A conversations afterwards. Each year, two Trainees or Junior Scientists are given the opportunity to present a talk and this year Ravi Sheth and Yinhu Wang were selected. This event provides the valuable moments for junior scientists to meet and engage in meaningful dialogue with the scientists who have defined IBD research because of their innovative work. The academic institutions of the Icahn School of Medicine at Mount Sinai, The Rockefeller University, NYU Langone Health, and Weill Cornell Medicine all provided sponsorship for this event. Generous sponsorship was also received from Boehringer Ingelheim, Janssen, the NY Crohn’s Foundation, the Kenneth Rainin Foundation, Cure for IBD, Pfizer, and Regeneron and in total, these contributions made the enriching day possible.


Dr. Chun-Jun Guo Receives NIH New Innovator Award

Dr. Chun-Jun (“C.J.”) Guo, an assistant professor of immunology in medicine in the Division of Gastroenterology and Hepatology and scientist at the Jill Roberts Institute for Research In Inflammatory Bowel Disease at Weill Cornell Medicine, has won a Director’s New Innovator Award from the National Institutes of Health (NIH) for an ambitious project to detail how the hundreds of different bacterial species living in the human gut contribute to human health and disease.

The NIH Director’s New Innovator Award, part of the NIH Common Fund, was established in 2007 to support “exceptionally creative early-career investigators who propose innovative, high-impact projects.” The award provides $1.5 million up-front to scientists, plus additional funds for university overhead costs, and is intended to support research programs lasting five years. Dr. Guo is among 60 scientists nationwide to receive the prestigious award this year.

“I’m very grateful for this award,” Dr. Guo said. “It provides my lab with a unique and exciting opportunity to pursue high-risk, high-reward research that would not get funding through traditional NIH grant mechanisms.”

Dr. Guo is an expert on the genetic manipulation of gut microbes. The diverse population of microbes in the human gut—the gut “microbiome”—has become a major focus of research in the past decade, as scientists have recognized it as a factor in major illnesses including inflammatory bowel disease, arthritis, diabetes and cancer. But determining in molecular detail what the roughly 1,000 species of gut microbes do to trigger disease or help maintain human health is an enormous undertaking. To read more, click here.


Weill Cornell Investigator Receives Inaugural Cancer Research Institute STAR Award

Dr. Gregory F. Sonnenberg, an associate professor of microbiology and immunology in medicine in the Weill Department of Medicine’s Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine, has been named an awardee for the inaugural CRI Lloyd J. Old STAR (Scientists Taking Risks) Program by the Cancer Research Institute.

The STAR program recognizes immunologists who are conducting high-risk, high-reward research in tumor immunology. Dr. Sonnenberg is one of five scientists to receive the honor following an international competition. As a recipient, he will receive a $1.25 million, five-year grant, to explore disruptive and uncommon cancer research paths. The CRI Lloyd J. Old STAR Award was named after the Cancer Research Institute’s founding medical and scientific director Lloyd J. Old, who was known as the “father of modern tumor immunology.”

“This is an incredible grant from a scientist’s standpoint,” Dr. Sonnenberg said. “Traditionally, this level of funding only comes from the National Institutes of Health. The Cancer Research Institute is really trusting us to take risks and make rapid scientific advances.”

Dr. Sonnenberg’s lab focuses on the immune system and its interaction with the body’s gut microbiome, which comprises trillions of microorganisms in the gastrointestinal tract. With this grant, he plans to examine the relationship between the immune system, microbiome and cancer. To read more, click here.


Discovery May Open Up New Possibilities for Treating Allergic Inflammatory Diseases

A molecule best known for its association with migraines may be a key to new treatments for common worm infections as well as allergic inflammatory disorders such as asthma, according to a study from scientists at Weill Cornell Medicine and the National Institutes of Health (NIH).

The scientists, whose work was published July 25 in Immunity, found a subset of white blood cells that reside in the lungs of mammals and produce the molecule, called CGRP, during worm infection in mice. The researchers discovered that the effect of CGRP in this context is to restrain the main immune response against the worms, known as a type 2 immune response. In the absence of CGRP signaling, this response is stronger and the worm infection ends more quickly.

The discovery suggests that CGRP-blocking drugs, developed in recent years to treat migraines, might also be useful in treating worm infections, which affect more than a billion people globally. Just as importantly, the findings hint that future drugs enhancing CGRP signaling could be useful against common inflammatory disorders such as asthma, food allergy and atopic dermatitis, which are caused by excessive type 2 immune responses. To read more, click here.


Weill Cornell Medicine celebrates Dr. Randy Longman’s appointment as new Center Director

Photo above: The reception to honor the appointment of Dr. Randy Longman. Pictured (L to R): Dr. Randy Longman, Jill Roberts, Dr. Anthony Hollenberg, Dr. Ellen Scherl, Dr. Charles Maltz, Dr. David Cohen, Dr. Dana Lukin, Dr. Julie Blander and Dr. David Artis.

Photo below: Dr. Randy Longman speaking at the reception. Photo credit: Tina Aswani Omprakash

On June 11, 2019, the WCM Division of Gastroenterology and Hepatology hosted a reception to congratulate Dr. Randy Longman, the newly appointed Director of the Jill Roberts Center for Inflammatory Bowel Disease (JRC), and honor the Center’s Founding Director, Dr. Ellen Scherl.

The JRC is one of the premier IBD centers for patient care and clinical research, and is composed of a team of gastroenterologists, surgeons, rheumatologists and hepatologists. Dr. Randy Longman joined the JRC in 2013. His role at the Center includes directing JRC activities, providing patient care and developing clinical and translational research that Dr. Longman passionately champions as a key approach to finding new treatments for IBD patients.

Dr. Longman is also a member of the Jill Roberts Institute for Research in IBD (JRI), where he leads a basic and translational IBD research program. He also contributes to JRI research activities including the WCM Microbiome Initiative and the JRC-JRI IBD Live Cell Bank.

Dr. David Cohen, the GI Division Chief, provided opening remarks, followed by Dr. David Artis, the Director of the JRI, Dr. Fabrizio Michelassi, Chairman of Surgery at WCM, Dr. Anthony Hollenberg, Chairman of Medicine at WCM, and Dr. Ellen Scherl, the Founding Director of JRC who all spoke warmly about Dr. Longman’s contributions and achievements.

The reception marks a new chapter in the JRC-JRI partnership in basic, clinical and translational IBD research and care, which could have never been possible without the unwavering support and vision of Jill Roberts, who attended the reception.

To learn more about the Jill Roberts Center for IBD, please click here. 

For the WCM Press Release, please click here.


Discovery Reveals Potential New Pathway for Treating Obesity and Related Disorders

A molecule that helps prevent fat accumulation in mammals is produced within fat tissues by stem-like cells that may be therapeutic targets for obesity and related disorders, according to a new study from scientists at Weill Cornell Medicine.

Obesity has become a global pandemic in recent decades, and presently affects more than 90 million Americans and hundreds of millions of people worldwide. Obesity can be debilitating on its own, but it also increases the risk of other major diseases including cancers, heart disease, diabetes and immunological disorders.

One molecule of interest for anti-obesity strategies is the signaling protein interleukin-33 (IL-33), which, in mice, acts on immune cells within fat tissues to dampen inflammation and curb obesity during overfeeding. IL-33 is thought to have the same effect on humans, in whom lower blood levels of IL-33 have been linked to higher body weight. The principal source of beneficial IL-33 in fat tissues has been a mystery, but the investigators, in their study published May 3 in Science Immunology, identified that source as a population of immature, fat-resident cells called adipose stem and progenitor cells. To read more, click here.


Inaugural Society for Mucosal Immunology Trainee Symposium for Local Chapter NYC hosted by the JRI

The Jill Roberts Institute hosted the Inaugural Society for Mucosal Immunology Symposium for Local Chapter NYC, organized by Drs. Iliyan Iliev and Gregory Sonnenberg. The symposium was sponsored by the Society for Mucosal Immunology. The event was filled to capacity and attendees listened to presentations from junior scientists, representing local New York City institutions working in Mucosal Immunology, including Columbia University, the Icahn School of Medicine at Mt. Sinai, Memorial Sloan Kettering Cancer Center, The Rockefeller University, Rutgers University, the Skirball Institute at New York University, and Weill Cornell Medicine. Drs. Iliev and Sonnenberg were pleased to include Keynote Speakers Dr. Miriam Merad from Icahn School of Medicine at Mt. Sinai and Dr. Dan Littman from the Skirball Institute at New York University on the event program to round out the strong presentations.  It provided a valuable opportunity to the junior scientists to present their research and to speak to a large audience. Most importantly, it provided an invaluable opportunity to develop connections and future fruitful collaborations among NYC-based institutions to further advance scientific discovery in the field of mucosal immunology. We are grateful for the financial support of the Society for Mucosal Immunology, The Office of the Dean at WCM and the JRI.

 


New York Academy of Science Awards Prize to JRI’s Dr. Xin Li

Photo: Dr. Bart Lambrecht (Left) and Dr. Xin Li (right) attending the New York Academy of Sciences "Severe Asthma, Inflammation, and Lung Repair” Conference

The Jill Roberts Institute is pleased to announce that Dr. Xin Li, a Postdoctoral Associate in the Iliev Lab, has been awarded the Outstanding Presentation Prize for his presentation, Sensing Fungal Dysbiosis by Gut-Resident CX3CR1+ Mononuclear Phagocytes Aggravates Allergic Airway Disease from the New York Academy of Sciences and F1000 (Faculty 1000). The award was presented during the “Severe Asthma, Inflammation, and Lung Repair” Conference held on Friday, April 26, 2019. The director of the Jill Roberts Institute, Dr. David Artis, also presented his talk, Regulation of Chronic Inflammation, at the event, details of which can be found here: https://www.nyas.org/events/2019/severe-asthma-novel-concepts-therapeutics/. This event included outstanding immunologists that travel from around the world to New York City. One of the highlights of the event was the closing Keynote Address, Charcot-Leyden Protein Crystals: From Marker of Death to a Drug Target in Asthma, presented by Dr. Bart N. Lambrecht, who is a key leader in the field of asthma and lung research working at Ghent University. 


Researchers Discover New Pathway Regulating Intestinal Health that is Impaired in Children with IBD

Image Credit: A color enhanced image of the healthy small intestine where immune cells and epithelial cells are highlighted in green and red. Image credit: Sonnenberg Lab

Production of an essential protein for maintaining a healthy immune response in the intestine called interleukin-2 (IL-2) depends on immune cells known as innate lymphoid cells (ILCs), according to a study by Weill Cornell Medicine researchers. The study, published April 3 in Nature, is the first to identify these cells and the factors that influence them as potential new targets for treating chronic gut inflammation associated with inflammatory bowel disease or food allergies.

“We have understood for quite a while that IL-2 is important for maintaining a healthy immune response in the gut,” said senior author Dr. Gregory Sonnenberg, an associate professor of microbiology and immunology in medicine in the Division of Gastroenterology and Hepatology and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. “Dramatic inflammation occurs when humans or mice are missing IL-2, but the specific cells that make it and the regulatory pathways controlling its production in the intestine were previously unknown.” To continue reading, click here.


CURE For IBD presents donation in continuing partnership with Jill Roberts Institute

Pictured in above image (L to R): Ron Kazel, Joe Lepler, Lina Krivyan, Drs. Ellen Scherl and David Artis, Jill Roberts, Patti Kaufman, Dr. Tom Haverty, Kyla Reicin

Since 2017, the Jill Roberts Institute for Research in Inflammatory Bowel Disease (IBD) and its Director, Dr. David Artis, have partnered with Chris Pedicone, Founder and President of CURE for IBD for a fruitful collaboration between laboratory research and dedicated fundraising efforts to find a cure for inflammatory bowel disease. CURE for IBD is a volunteer non-profit organization devoted solely to funding IBD research that seeks new treatments and cures for family, friends, and others living with IBD. On February 4, 2019, the CURE for IBD team, including Ron Kazel, Joe Lepler, Lina Krivyan, Patti Kaufman, Dr. Tom Haverty and Kyla Reicin, visited the Jill Roberts Institute for discussion and a tour of the laboratory facilities. At the close of their visit, CURE for IBD graciously presented the Jill Roberts Institute with a check for $75,000 to support IBD research efforts. Dr. Artis and members of the Jill Roberts Institute extend their gratitude to CURE for IBD and celebrate this ongoing partnership that supports current and future IBD research efforts.


Researchers Create the First Anatomical Map of Innate Lymphoid Cells in Healthy Human Tissues

Image credit: This heat map represents the low (blue) and high (red) gene expression of innate lyphoid cells in the body. Credit: Dr. Laurel Monticelli

Researchers have long known that dysfunction in the body’s innate immune system breaks the first line of defense against invading pathogens, enabling diseases to flourish unchecked. However, scientists’ ability to enhance the protective features of the innate immune system has been hampered by a lack of information about what a ‘healthy’ innate immune system looks like in different sites throughout the human body.

Now, in findings published Feb. 12 in Immunity, Weill Cornell Medicine investigators have been the first to generate an anatomical ‘map’ detailing the distribution of innate lymphoid cells in tissues from previously healthy humans. By establishing a baseline of immune activity, this study provides important insights into how the healthy immune system functions in an organ-specific way. This knowledge can be used to aid scientists in developing more effective treatments for a range of immunological diseases including infection, autoimmunity, and cancer. To read more, click here.


Researchers Identify Critical Role for Protein in Colon Inflammation

A protein induced by gut microbes is vital in healing colons that have become inflamed due to a short-term form of colitis, Weill Cornell Medicine researchers discovered in a new study. However, they also found that this molecule, called TNF-like ligand 1A (TL1A) contributes to the sustained inflammation characterized by chronic inflammatory bowel disease (IBD).

In a study published Dec. 11 in Immunity, Dr. Randy Longman, an assistant professor of medicine in the Division of Gastroenterology and Hepatology and a researcher in the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine, and his colleagues investigated colitis in mice and humans to better understand how immune cells communicate to help heal the inner-most layer of the intestinal tract, called the mucosal barrier. Developing a better understanding of the molecular factors that contribute to IBD may one day help clinicians more accurately diagnose and treat patients, Dr. Longman said. About 1.6 million people in the United States have IBD, 907,000 of whom have ulcerative colitis. To read more, click here.


Daedalus Fund Supports Eight Investigators

Photo credit: Dr. Augustine M.K. Choi, the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine (second from left), and Larry Schlossman, managing director of BioPharma Alliances and Research Collaborations at Weill Cornell Medicine (first from left), join the winners of the Daedalus Fund for Innovation awards. From third from left: Dr. Shahin Rafii, Dr. Matthew Greenblatt, Dr. Lew Cantley, Dr. Julie Blander, Dr. Juan Cubillos-Ruiz, Dr. Peter Goldstein, Dr. Barbara Hempstead and Dr. Steven Lipkin.

Eight Weill Cornell Medicine faculty members have been selected for the fifth round of the Daedalus Fund for Innovation awards, a pioneering institutional program that helps advance promising applied and translational research projects and emerging technologies that have commercial potential. Awardees are chosen twice annually and are eligible for two levels of funding: $100,000 and $300,000 (the latter, subject to the satisfaction of certain specified pre-defined milestones).

The researchers — Drs. Julie Blander, Lew Cantley, Juan Cubillos-Ruiz, Peter Goldstein, Matthew Greenblatt, Barbara Hempstead, Steven Lipkin and Shahin Rafii — have each won a Daedalus award to fund proof-of-concept studies that will enhance the data package, thereby helping to upgrade their technologies and translate their early-stage discoveries into new therapeutic modalities and hopefully more effective treatments for patients. To read more, click here.


Sensing of Fungi by Gut Immune Cells Can Contribute to Airway Allergic Diseases

Common drug treatments that lead to changes in gut fungi can persistently exacerbate allergic airway diseases such as asthma, according to a study by Weill Cornell Medicine researchers.

The study, published online Nov. 29 in Cell Host & Microbe, suggests that the enormous modern prevalence of allergic airway diseases may be attributable in part to the widespread use of antimicrobials, including antifungals and other therapies that disrupt the normal balance between bacterial and fungal species in the gut.

“We were able to identify gut-resident immune cells that sense fungal community imbalance in the intestines and transmit these immune signals to the lung contributing to aggravated allergy,” said senior study author Dr. Iliyan D. Iliev, an assistant professor of immunology in medicine in the Division of Gastroenterology and Hepatology and a researcher in the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. To read more....


Gift establishes Friedman Center for Nutrition and Inflammation

With a $7.5 million gift from the Friedman Family Foundation, endowed by Stephen and Vice Chair Overseer Barbara Friedman, Weill Cornell Medicine has established an innovative cross-campus center dedicated to improving human health through research in the complex relationship between nutrition, inflammation and the development of disease.

The Friedman Center for Nutrition and Inflammation will create new programs across Weill Cornell Medicine and Cornell’s Ithaca campus, harnessing key resources to study the interaction between diet, the immune system and the microbiome – the genetic material generated by the viruses, bacteria, fungi and parasites that live in or on the human body.

The two Cornell campuses are working together to engage other donors to match the support provided by the Friedmans and the Friedman Family Foundation with the vision of a $15 million initiative that will foster groundbreaking research and provide state-of-the-art education in nutrition, inflammation and the microbiome for medical and graduate students and clinicians.

The Friedman Center will be directed by Dr. David Artis, a world leader in immunology, inflammation and microbiome research. He is director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease and the Michael Kors Professor in Immunology at Weill Cornell Medicine.

Researchers at the center will work to develop treatments and preventive strategies for illnesses including cancer, arthritis, Alzheimer’s disease, diabetes and inflammatory bowel disease – virtually every disease area represented in the Belfer Research Building, says Dr. Artis. To read more, click here.


New Faculty Recruit to the Jill Roberts Institute Will Explore How the Human Microbiota Regulates Health and Disease

Dr. Chun-Jun Guo is a newly appointed faculty member to the Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Department of Medicine at Weill Cornell Medicine. His lab is located on the 7th floor of Belfer Research Building and his research program focuses on studying the molecular mechanisms behind host-microbe interaction in the context of health and disease.

Before joining JRI-WCM, Dr. Guo was a postdoctoral scholar at Professor Michael Fischbach’s lab at Stanford working on the small molecules from the bacteria living in the human intestine, commonly known as ‘the human gut microbiota’. These molecules are highly abundant, circulatory, and few of them are well-known ligands for host receptors. However, the biology of the majority of them still remains elusive. Dr. Guo developed the first CRISPR-Cas9-based system in a gut commensal Clostridium sporogenes that is previously challenging to be genetically modified. By mutating the biosynthetic genes for a metabolite and using mouse models, Dr. Guo is able to toggle on/off the production of these abundant microbiome-derived small molecules in the host and use this tool to investigate their effects on host biology and IBD progression. To continue reading, click here...


2018 NYC IBD Day Held at New York University Langone Health

On September 12, 2018, the 4th Annual New York City IBD Research Day was hosted by New York University Langone Health in the Farkas Auditorium. This yearly symposium is a collaborative effort of four institutions: The Jill Roberts Institute at Weill Cornell Medicine, The Immunology Institute of the Icahn School of Medicine at Mount Sinai, The Center for Basic and Translational Research on Disorders of the Digestive System at The Rockefeller University and The Skirball Institute and the Departments of Medicine and Surgery at New York University Langone Health. The big announcement this year was that Columbia University will join this group of institutions, hosting the 2019 NYC IBD Day. In honor of the late Lloyd F. Mayer, MD, there is a Mayer Prize given yearly. Dr. Sergio Lira presented the Mayer Prize to his friend and colleague, Dr. Dan Littman. Throughout the course of the day, the attendees listened to ten presenters, who had traveled from around the globe for this event, engaging in lively Q & A conversations afterwards. This year, Irina Leonardi, a Postdoctoral Associate from the Jill Roberts Institute, was invited to be a speaker in the highly-regarded program. She presented a seminar entitled, “Immune Recognition of the Intestinal Mycobiota.” Generous sponsorship from The Helmsley Charitable Trust, the NY Crohn’s Foundation, the Kenneth Rainin Foundation, Cure for IBD, Pfizer, Boehringer Ingelheim, Regeneron, and Janssen made the enriching day possible.


Identifying pathways that control the location and function of immune cells in the intestine

Group 3 innate cells (red staining with green staining in the center) are found in between B cell follicles (grey staining) where immune responses take place in gut-associated lymph nodes. Picture courtesy of Dr. David Withers.

The intestinal mucosal barrier surface is constantly exposed to various stimuli such as food antigens, beneficial microbes, and infectious pathogens. Immune cells in the intestine and associated lymphoid tissues play a critical role in maintaining barrier function and intestinal homeostasis.

A new study by Dr. David Artis and his colleagues at Weill Cornell Medicine, identifies that the accumulation and function of group 3 innate lymphoid cells, a key immune cell population that limits bacterial infections in the intestine, are regulated by G protein-coupled receptor 183 (GPR183) and its ligand oxysterol produced by stromal cells. The study is co-authored by multiple investigators including Dr. Gregory F. Sonnenberg (Weill Cornell Medicine) and Dr. David Withers (University of Birmingham) and was published on June 26, 2018 in Cell Reports.

“Group 3 innate lymphoid cells are enriched in mucosal barrier surfaces and lymphoid tissues, and are a key immune cell in maintaining intestinal health against bacterial infections,” said Dr. Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease and the Michael Kors Professor of Immunology at Weill Cornell Medicine. “However, the molecular mechanisms that control how group 3 innate lymphoid cells are distributed in the intestine and lymphoid tissues and how their functions are controlled during bacterial infection are not fully understood.”

For their study, Dr. Artis and his colleagues focused on a G protein-coupled receptor 183 (GPR183, also known as EBI2). GPR183 is highly expressed on lymphocytes in spleen and lymph nodes and controls cell migration to achieve efficient antibody responses and CD4+ T cell responses. Dr. Artis and his team found that group 3 innate lymphoid cells, not only in gut-draining lymph nodes but also in the intestine, highly expressed GPR183 that controls the distribution of group 3 innate lymphoid cells in these tissues. Furthermore, GPR183 ligand, 7α,25-dihydroxycholesterol was produced by gut stromal cells, supporting a role for these structural cells in controlling the location and functional potential of group 3 innate lymphoid cells.

To examine the role of GPR183 and its ligand, Dr. Artis and his team employed mice that lack the receptor and the ligand-producing enzyme CH25H and found disorganized accumulation of ILC3s in the gut-draining lymph nodes and reduced ILC3 accumulation in the intestine in the absence of GPR183 or its ligand. “Considering the regulation of lymphocytes by ILC3s in the lymphoid organs and the importance of immune cell localization in these organs, it is important to know how ILC3 localization is controlled in the lymph nodes. And our findings may provide new targets to control immune responses in the lymphoid organs,” said Dr. Coco Chu, a postdoctoral associate in Dr. Artis’ laboratory and a co-first author of the study.

“We then wanted to know if this GPR183 is essential for a protection against gastrointestinal pathogens,” said Dr. Saya Moriyama, a postdoctoral associate in Dr. Artis’ laboratory and another co-first author of the study. To examine this, Dr. Artis and his colleagues used Citrobacter rodentium infection, which is a gastrointestinal pathogen of mice that has several pathogenic similarities with clinically important human gastrointestinal pathogens. “And we found that GPR183 promotes accumulation of cytokine-producing group 3 innate lymphoid cells in the gut and is required for protection against this infection.,” she added.

GPR183 plays important roles in regulating the distribution and function of ILC3s in both lymphoid and non-lymphoid tissue so GPR183 and its oxysterol ligand-producing pathway could be potential therapeutic targets for controlling and regulating ILC3 functions in multiple infectious and inflammatory diseases.

This study was supported by grants from the National Institutes of Health (DP5OD012116, AI123368, DK110262, AI095608, AI074878, AI083480, AI095466, AI095608, AI102942, AI097333 and AI106697), the German Research Foundation (KL 2963/1-1), the Novo Nordic Foundation (14052), the Jill Roberts Institute, the Wellcome Trust (Senior Research Fellowship 110199/Z/15/Z), Cure for IBD, the Crohn’s and Colitis Foundation of America, the Searle Scholars Program, an American Asthma Foundation Scholar Award, the Burroughs Wellcome Fund. Dr. Moriyama is also the Japanese Society for the Promotion of Science Overseas Research Fellow.


Weill Cornell Medicine Opens New Microbiome Core

The Jill Roberts Institute for Research in Inflammatory Bowel Disease is now home to Weill Cornell Medicine’s new Microbiome Core, https://www.microbiome.weill.cornell.edu/,which officially opens June 1. The core’s mission is to provide researchers with the technological platforms required to perform microbiome sequencing and analysis.

A microbiome is the aggregate of microorganisms living in an environment and the human microbiome consists of microorganisms that live in the human body.

“There’s a major biomedical revolution right now in understanding how the microbiome contributes to disease, and we are excited to be a part of that,” said Dr. Randy Longman, an assistant professor of medicine and a gastroenterologist at the Jill Roberts Center for Inflammatory Bowel Disease. “Now scientists are researching how the microbiome plays a role in normal development, the function of the immune system, metabolism, and the susceptibility to diseases including allergies, arthritis, cancer, inflammatory bowel disease and more.” To continue reading...


Modified Inactivated Vaccine May Produce Immune Response as Effective as Live Vaccine

Vaccines containing inactivated versions of disease-causing germs are traditionally not as effective as live vaccines made with weakened pathogens. But new research from Weill Cornell Medicine scientists reveals how a molecule found in live vaccines produces a robust immune response, and adding it to an inactivated vaccine can create the same strong results.

These insights may provide a blueprint for engineering more potent inactivated or “dead” vaccines that can deliver strong immunity while overcoming concerns about the health risks of live vaccines.

“There has been a reluctance in the general population to get vaccinated, but vaccines are the single most effective medical intervention proven to prevent disease,” said senior author Dr. Julie Magarian Blander, a senior faculty member in the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine, who was recruited as a professor of immunology in medicine. “We have known that live vaccines provide better protection, often for life, in one dose, compared to dead vaccines that frequently require multiple doses or boosters over time.” To continue reading...


Nervous System Puts the Brakes on Inflammation

Mucus production (red) in the lung under inflammatory conditions. Picture courtesy of Dr Saya Moriyama.

Cells in the nervous system can “put the brakes” on the immune response to infections in the gut and lungs to prevent excessive inflammation, according to research by Weill Cornell Medicine scientists. This insight may one day lead to new ways to treat diseases caused by unchecked inflammation, such as asthma and inflammatory bowel disease.   

The study, published March 1 in Science, provides some clues about what might be going wrong in these diseases, which have become more common in industrialized countries, and in helminth infections, which are still a major public health problem in less-industrialized countries. It also may explain how some existing treatments for diseases like asthma work and point to new treatment strategies.

“There is a crosstalk between the nervous system and the immune system, and that plays an important role in regulating acute and chronic inflammation,” said Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease and the Michael Kors Professor of Immunology at Weill Cornell Medicine. “Those two organ systems are closely interacting and play an important role in human health and disease.” To continue reading...


Scientists Identify Immune Cells That Keep Gut Fungi Under Control

Photo above shows opportunistic fungus called candida albicans (red) engulfed by CX3CR1+ phagocytes (green) in the gut villi (blue). Photo credit: Dr. Iliyan Iliev and Dr. Irina Leonardi.

Immune cells that process food and bacterial antigens in the intestines control the intestinal population of fungi, according to a new study from Weill Cornell Medicine scientists. Defects in the fungus-fighting abilities of these cells may contribute to some cases of Crohn’s disease and other forms of inflammatory bowel disease (IBD).

The findings, published Jan. 11 in Science, illuminate a strong connection between fungi, immunity and intestinal inflammation and suggest a new, targeted treatment strategy for IBD.

“After discovering that fungi might be involved in the pathology of IBD, one of the big questions in the field has been how to identify patients who would benefit from antifungal co-therapy, and our finding suggests a way to do that,” said senior author Dr. Iliyan Iliev, an assistant professor of microbiology and immunology in medicine at Weill Cornell Medicine and a scientist at the Jill Roberts Institute for Research in Inflammatory Bowel Disease. To continue reading...


The Jill Roberts Institute plays starring role in the treatment of a young actress living with Crohn's Disease

When Analise Scarpaci was 10-years-old, she dreamed of singing and dancing on famed Broadway stages. So when she was diagnosed with a form of inflammatory bowel disease called Crohn’s disease, she wasn’t going to let that obstacle stand in her way. Thanks to her doctors at Weill Cornell Medicine and NewYork-Presbyterian, Scarpaci, now 18 and a Broadway star, is able to manage her disease and contribute to researchers’ understanding of the genetic and immunological underpinnings of IBD—all the while pursuing what she loves.


CURE For IBD presents donation to Jill Roberts Institute for research funding

Pictured in above image (L to R): Ms. Patti Kaufman, Dr. Robbyn Sockolow, Dr. David Artis, Dr. David Cohen, Mr. Chris Pedicone, and Ms. Lina Krivyan

On November 15, 2017, the Jill Roberts Institute for Research in Inflammatory Bowel Disease (IBD) and its Director, Dr. David Artis, welcomed Chris Pedicone, Founder and President of CURE for IBD for a visit and tour of the IBD research facilities at Weill Cornell Medicine. Joining the visit were Patti Kaufman, a Trustee and Fundraiser and Lina Krivyan, also a Fundraiser at CURE for IBD. CURE for IBD is a volunteer non-profit organization devoted solely to fund IBD research in order to find new treatments and cures for family, friends, and others living with IBD. This notable moment would not have been possible without Jill Roberts, a long-term supporter of IBD research and patient care at Weill Cornell Medicine. CURE for IBD presented the Jill Roberts Institute with a check for $35,000 to support IBD research efforts. Dr Artis and members of the Jill Roberts Institute extended their sincere thanks to CURE for IBD and are delighted to partner with CURE for IBD to support ongoing and future IBD research efforts at Weill Cornell Medicine. 


NYC IBD Research Day 2017

On November 2, 2017, the 3rd Annual New York City IBD Research Day was hosted by The Rockefeller University on their campus. The symposium is a yearly event coming to fruition through the collaboration of three institutions: The Jill Roberts Institute at Weill Cornell Medicine, The Immunology Institute of the Icahn School of Medicine at Mount Sinai, and The Center for Basic and Translational Research on Disorders of the Digestive System at The Rockefeller University. Dr. Bana Jabri graciously accepted the Lloyd D. Mayer, MD Award presented by her friend and colleague, Dr. Sergio Lira. The attendees listened to ten presenters, who had traveled from around the globe for this event, engaging in lively Q & A conversations afterwards. Generous sponsorship from The Helmsley Charitable Trust, the NY Crohn’s Foundation, the Kenneth Rainin Foundation, Pfizer, and Boehringer Ingelheim made the enriching day possible.


A Cellular Tango: Immune and Nerve Cells Work Together to Fight Gut Infections

Nerve cells in the gut play a crucial role in the body’s ability to marshal an immune response to infection, according to a new study from Weill Cornell Medicine scientists.

The study, published Sept. 6 in Nature, shows that the immune system and nervous system have co-evolved to respond to infectious threats. This means that scientists looking for ways to treat diseases like inflammatory bowel disease or asthma that involve an excessive immune system response may also have to address the nervous system’s role. 

“The immune system and neuronal system don’t act independently,” said senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease and the Michael Kors Professor of Immunology at Weill Cornell Medicine. “They are working together.”

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Dr. Gregory Sonnenberg Wins Inaugural Award from the Society for Mucosal Immunology

Dr. Gregory Sonnenberg, an assistant professor of microbiology and immunology at Weill Cornell Medicine, has received the newly established Young Investigator Award from the Society for Mucosal Immunology.

The award honors investigators within 15 years of their postdoctoral training who have made significant contributions to the field of mucosal immunology, which is the study of immune responses that occur in the intestines, lungs and urogenital tract.

Dr. Sonnenberg accepted his award at the 18th International Congress of Mucosal of Immunology on July 19 in Washington, D.C. The award carries a cash prize and additional funds to support Dr. Sonnenberg’s laboratory.

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Research Uncovers Bacteria Linking Crohn’s Disease to Arthritis

Patients with Crohn’s disease, a type of inflammatory bowel disease (IBD) that causes abdominal pain and diarrhea, can also experience joint pain. In Crohn’s disease, which affects about 800,000 Americans, the immune system can attack not only the bowels, but the musculoskeletal system as well, leading to spondyloarthritis, a painful condition that affects the spine and joints. Now new research, published Feb. 8 in Science Translational Medicine, helps explain the connection between these seemingly unrelated symptoms, and could help physicians identify Crohn’s disease patients who are more likely to develop spondyloarthritis, enabling them to prescribe more effective therapies for both conditions.

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Cell Death in Gut Implicated in IBD

The natural lifecycle of cells that line the intestine is critical to preserving stable conditions in the gut, according to new research led by a Weill Cornell Medicine investigator. The findings may lead to the development of new therapies to alleviate inflammatory bowel disease (IBD) and other chronic inflammatory illnesses.

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Kenneth Rainin Foundation Awards $750,000 for Collaborative Inflammatory Bowel Disease Research Projects

OAKLAND, Calif., Feb. 14, 2017 /PRNewswire-USNewswire/ -- The Kenneth Rainin Foundation announced today that it has awarded $750,000 for Inflammatory Bowel Disease (IBD) research through its Synergy Award program. The Rainin Foundation funds scientific projects that have the potential to yield transformative discoveries and major insights into predicting and preventing IBD.

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Investigator Wins Award to Continue Study of Fungi in Inflammatory Bowel Disease

Dr. Iliyan Iliev, an assistant professor of immunology in medicine at Weill Cornell Medicine, has been awarded a one-year, $100,000 grant from the Kenneth Rainin Foundation to study the behavior of fungi in the immune system when patients with inflammatory bowel disease are administered a form of immunotherapy.  

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NYC IBD Research Day 2016

New York City IBD Research Day, on Nov 7, 2016, was a success.  Over 200 attendees enjoyed presentations on a variety of research presented by a multitude of lecturers from around the globe. The symposium was a one day event hosted by the Jill Roberts Institute at the Weill Cornell Medicine Belfer Research Building, in collaboration with the Immunology Institute of the Icahn School of Medicine at Mount Sinai, and the Center for Basic and Translational Research on Disorders of the Digestive System at The Rockefeller University. Dr. Richard Blumberg of Harvard Medical School was presented with the Lloyd F. Mayer, MD award.


The Fungus Among Us

NEW YORK (July 25, 2016) - By now, most of us have made peace with the fact that we are host to a complicated extended family of bacteria whose trillion-plus members give us vitamins, help us digest food, protect us from pathogens, and only rarely turn virulent on us. But what about the fungus among us?

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Disruption of Intestinal Fungi Leads to Increased Severity of Inflammatory Disease

Fungi that live in a healthy gut may be as important for good health as beneficial intestinal bacteria, according to new research conducted at Weill Cornell Medicine.

Scientists have known for quite some time that the so-called "good" gut bacteria in the intestines, known as commensal bacteria, are a key component of a healthy body. These bacteria are critical for proper digestive and immune system function. Recent discoveries, however, have indicated that other microbes, such as fungi and viruses, may also play a part in how the body handles inflammation.

Continue reading at: http://weill.cornell.edu/news/news/2016/06/disruption-of-intestinal-fung...


An Off-Switch for Allergy: Starving the Immune System Prevents Allergic Inflammation in the Lung

NEW YORK (April 4, 2016) — Starving immune cells of key nutrients stymies their ability to launch an allergic response, according to new research from a multi-institutional collaboration led by Weill Cornell Medicine investigators. The findings illuminate how nutrients help drive tissue inflammation caused by the immune system — an insight that could lead to new treatments for a wide range of inflammatory conditions from hay fever and food allergies to asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF).

Continue to read at: http://weill.cornell.edu/news/news/2016/04/an-off-switch-for-allergy-sta...


Bacteria in Immune Cells May Protect Against Chronic Inflammation

NEW YORK (March 15, 2016) — A population of bacteria inhabits human and mouse immune cells and appears to protect the body from inflammation and illness, Weill Cornell Medicine scientists discovered in a new study. The findings challenge conventional wisdom about the relationship between bacteria and the human body — and about how the microbes influence health and disease. The study, published March 15 in Immunity, focused on "good" or "commensal" bacteria that live in the human intestine and are essential for digestion and proper immune function.

Continue reading at: http://weill.cornell.edu/news/news/2016/03/bacteria-in-immune-cells-may-...


Innovative Therapeutic Approach Shows Promise in Treating Inflammatory Bowel Disease

NEW YORK (February 16, 2016) — An investigative therapy given to mice blocks the overactive immune responses that are a hallmark of inflammatory bowel disease without impairing the body's ability to fight infection, an international research team led by Weill Cornell Medicine investigators finds in a new study. The preclinical discovery may lead to more effective treatment strategies for IBD.

Continue to read at: http://weill.cornell.edu/news/news/2016/02/hed-innovative-therapeutic-ap...


Restoring "Gut Health" in Patients with Inflammatory Bowel Disease May Be a Matter of Pushing Cells to Repair Our Tissues

NEW YORK (August 04, 2015) — New insight into how the intestines repair themselves after daily attacks from microbes and other environmental triggers could lead to innovative approaches to treating inflammatory bowel disease, according to new research by Weill Cornell Medical College investigators. The findings, published Aug. 4 in PNAS, reveal a mechanism that allows the single layer of cells that line the inside of the intestines, called the gut epithelium, to signal the immune system to repair tissue damage caused by the daily onslaught of microbes and other environmental factors that the body encounters. Because a defect in that repair system underlies Crohn's disease and ulcerative colitis, the two primary forms of IBD, restoring tissue-protective repair mechanisms could reduce the diseases' hallmarks, chronic inflammation and tissue damage.

Continue reading at: http://weill.cornell.edu/news/news/2015/08/restoring-gut-health-in-patie...


Weill Cornell Investigators Discover a New Pathway that Prevents Chronic Inflammation in the Gut

New York (April 23, 2015) — An international research team led by Weill Cornell Medical College investigators has discovered an answer to why the human immune system ignores roughly 100 trillion beneficial bacteria that populate the gastrointestinal tract. The findings, published April 23 in the journal Science, advance investigators' understanding of how humans maintain a healthy gastrointestinal tract, and may provoke new ways to treat inflammatory bowel disease — including Crohn's disease and ulcerative colitis — whose origins have been mysterious and treatment difficult.

Continue reading at: http://weill.cornell.edu/news/pr/2015/04/weill-cornell-investigators-dis...


Immune Cells in "White" Body Fat Limit Obesity, Researchers Say

In the Dec. 22 issue of Nature, a research team, led by investigators at Weill Cornell Medical College, has found that an immune cell type appears to help burn fat and prevent the development of obesity. The findings suggest new ways of possibly preventing or treating obesity and obesity-related diseases in humans, says the study's senior investigator, Dr. David Artis, an immunologist who leads the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell.

Continue reading at: http://weill.cornell.edu/news/news/2014/12/immune-cells-in-white-body-fa...


JRI Investigators Featured in Weill Cornell Medicine: Inside Medicine


Jill Roberts Institute for Research in Inflammatory Bowel Disease Leads the Field

NEW YORK (April 18, 2016) — A string of high-profile research studies underscores the early successes of the Jill Roberts Institute for Research in Inflammatory Bowel Disease, where scientists are assiduously investigating the root causes of the disease. Now, with the official opening of its permanent laboratories, the Weill Cornell Medicine institute is poised to lead the way in advancing research to improve patient care. Established nearly two years ago with a generous gift to Weill Cornell Medicine from longtime benefactor Jill Roberts, the institute uses a multidisciplinary approach to drive and then translate discoveries into new preventative and treatment strategies for IBD, a group of chronic inflammatory conditions of the intestine that affects an estimated 3.5 million people worldwide.

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New Jill Roberts Institute for Research in Inflammatory Bowel Disease Established at Weill Cornell Medical College

NEW YORK — Weill Cornell Medical College announced today that through the generosity of longstanding benefactor Jill Roberts and the Jill Roberts Charitable Foundation it is establishing the Jill Roberts Institute for Research in Inflammatory Bowel Disease. Dr. David Artis, one of the world's leading immunologists, was recruited from the University of Pennsylvania School of Medicine to direct the institute, which is dedicated to understanding the molecular underpinnings of inflammatory bowel disease with the goal of translating basic research breakthroughs into the most advanced therapies for patients.

Continue reading at: http://weill.cornell.edu/news/pr/2014/06/new-jill-roberts-institute-for-research-in-inflammatory-bowel-disease-established-at-weill-cornell-m.html


Weill Cornell Medicine The Jill Roberts Institute for Research in Inflammatory Bowel Disease 413 E 69th Street, 7th Floor New York, NY 10021 Phone: (646) 962-6312