Neurons that sense pain protect the gut from inflammation and associated tissue damage by regulating the microbial community living in the intestines, according to a study from researchers at Weill Cornell Medicine.

The researchers, whose report appears Oct. 14 in Cell, found in a preclinical model that pain-sensing neurons in the gut secrete a molecule called substance P, which appears to protect against gut inflammation and related tissue damage by boosting the population of beneficial microbes in the gut. The researchers also found that these pain-sensing nerves are diminished in number, with significant disruptions to their pain-signaling genes, in people who have inflammatory bowel disease (IBD).

“These findings reshape our thinking about chronic inflammatory disease, and open up a whole new approach 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 at Weill Cornell Medicine.

Dr. David Artis

The study’s first author, Dr. Wen Zhang, a postdoctoral researcher in the Artis laboratory, added, “Defining a previously unknown sensory function for these specific neurons in influencing the microbiota adds a new level of understanding to host-microbiota interactions.”

IBD covers two distinct disorders, Crohn’s disease and ulcerative colitis, and is believed to affect several million people in the United States. Typically it is treated with drugs that directly target elements of the immune system. Scientists now appreciate that gut-dwelling bacteria and other microbes also help regulate gut inflammation.

As Dr. Artis’s laboratory and others have shown in recent years, the nervous system, which is “wired” into most organs, appears to be yet another powerful regulator of the immune system at the body’s barrier surfaces. In the new study, Dr. Artis and his team specifically examined pain neurons that innervate—extend their nerve endings into—the gut.

Dr. Wen Zhang

These gut-innervating pain neurons, whose cell bodies sit in the lower spine, express a surface protein called TRPV1, which serves as a receptor for pain-related signals. TRPV1 can be activated by high heat, acid, and the chili-pepper compound capsaicin, for example—and the brain translates this activation into a sense of burning pain. The researchers found that silencing these TRPV1 receptors in gut nerves, or deleting TRPV1-expressing neurons, led to much worse inflammation and tissue damage in IBD mouse models, whereas activating the receptors had a protective effect.

The investigators observed that the worsened inflammation and tissue damage in TRPV1-blocked mice were associated with changes in the relative populations of different species of gut bacteria. When this altered bacterial population was transplanted into normal mice, it caused the same worsened susceptibility to inflammation and damage. By contrast, broad-spectrum antibiotic treatment could reverse this susceptibility even in TRPV1-blocked mice. This result demonstrated that TRPV1-expressing nerves protect the gut mainly by helping to maintain a healthy gut microbe population. To continue reading, click here.

Immune cells called group 3 innate lymphoid cells (ILC3s) play an essential role in establishing tolerance to symbiotic microbes that dwell in the human gastrointestinal tract, according to a study led by researchers at Weill Cornell Medicine.

The discovery, reported Sept. 7 in Nature, illuminates an important aspect of gut health and mucosal immunity—one that may hold the key to better treatments for inflammatory bowel disease (IBD), colon cancer and other chronic disorders.

“As part of this study, we define a novel pathway that drives immune tolerance to microbiota in the gastrointestinal tract,” said senior author Dr. Gregory F. Sonnenberg, associate professor of microbiology and immunology in medicine and head of basic research in the Division of Gastroenterology & Hepatology, and a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease at Weill Cornell Medicine. “This is a fundamental advance in our understanding of mucosal immunity and may hold the key to understanding what goes wrong when the immune system begins to inappropriately attack microbiota in diseases such as IBD.”

Drs. Mengze Lyu and Gregory Sonnenberg

Scientists have long known that trillions of bacteria, fungi, and other microbes dwell symbiotically in the intestines of mammals. The mechanism by which the immune system normally tolerates these “beneficial” gut microbes, instead of attacking them, has not been well understood. But there is evidence that this tolerance breaks down in IBD, leading to harmful flareups of gut inflammation. Thus, a detailed understanding of gut immune tolerance could enable the development of powerful new treatments for IBD—a class of diseases that include Crohn’s disease and ulcerative colitis, which affect several million individuals in the United States alone.

In the study, Dr. Sonnenberg and colleagues, including lead author Dr. Mengze Lyu, a postdoctoral researcher in the Sonnenberg lab, used single-cell sequencing and fluorescent imaging techniques to delineate immune cells in the mesenteric lymph nodes that drain the intestines of healthy mice. They focused on cells expressing a transcription factor, RORγt, which are known to drive either inflammation or tolerance in response to microbes that colonize the intestine. The dominant immune cell types in these tissues, they found, were T cells and ILC3s. The latter are a family of immune cells that represent an innate counterpart of T cells, and work as a first line of defense in mucosal tissues such as the intestines and lungs.

In close collaboration with researchers at the University of Birmingham, UK, the scientists observed that in lymph node regions called interfollicular zones, ILC3s are in close association with a specific type of T cell, called RORγt+ regulatory T cells (Tregs), which are adapted to dial down inflammation and immune activity to promote tolerance in the gut. To continue reading, please click here.

Two Weill Cornell Medicine physician-scientists, Dr. Randy Longman and Dr. Robert Schwartz, have been elected as members of the American Society for Clinical Investigation.

The American Society for Clinical Investigation (ASCI) is one of the nation’s oldest nonprofit medical honor societies and focuses on the unique role of physician-scientists in research, clinical care and medical education. It is comprised of more than 3,000 physician-scientists serving in the upper ranks of academic medicine and industry. Members are leaders in their fields in translating innovative laboratory findings into clinical advancements. Drs. Longman and Schwartz join 93 other new members elected this year and will be officially inducted at the organization’s annual meeting in April.

Dr. Randy Longman

Dr. Randy Longman is an associate professor of medicine in the Division of Gastroenterology and Hepatology at Weill Cornell Medicine and director of the Jill Roberts Center for Inflammatory Bowel Disease at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center. His research focuses on interactions between gut microbes and the immune system in inflammatory bowel disease (IBD). His work has identified specific strains of bacteria that are involved and how they relay signals to the immune system to activate inflammation in patients with Crohn’s disease and ulcerative colitis, the most common forms of IBD.

Dr. Longman is currently leading a clinical trial evaluating whether dietary fiber supplementation may improve the efficacy of fecal microbiota transplantation (FMT) in patients with moderate ulcerative colitis. Supported by the National Institute of Diabetes and Digestive and Kidney Diseases, the trial is based on his earlier work that identified specific microbes associated with clinical responses to FMT. Dr. Longman’s research is funded by several organizations, including the National Institutes of Health and the Crohn’s and Colitis Foundation.

“It’s very meaningful to be elected as a member of the ASCI, knowing my peers recognize my work has contributed toward moving the needle forward,” said Dr. Longman, who is also a member of the Jill Roberts Institute for Research in Inflammatory Bowel Disease. “As a physician-scientist, the most important thing for me is that my research discoveries may translate into clinical treatments that help patients.” To read further, click here.

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.

(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.

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

“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.

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.

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.

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.

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.

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.

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. 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.

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, Chair of Surgery at WCM, Dr. Anthony Hollenberg, Chair 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.

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.

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.

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.

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.

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.

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.

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...

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...

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.

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.

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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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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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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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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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...

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...

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...

Alex: Hope for Tomorrow from Weill Cornell Medicine on Vimeo.