Potential Approach to Decrease Immune Responses in IBD Suggested by BIDMC Researchers

Potential Approach to Decrease Immune Responses in IBD Suggested by BIDMC Researchers
In a new study entitled “NADH oxidase-dependent CD39 expression by CD8+ T cells modulates interferon gamma responses via generation of adenosine,” a team of researchers shed light on the role of the ecto-enzyme CD39 on immune cells and its regulatory action in inflammatory bowel disease (IBD). The study was published in the journal Nature Communications. IBD, including Crohn’s disease, is an immune disorder characterized by an excessive response of a particular group of immune cells called T cells. A specialized group of T cells known as CD8+ T cells release high amounts of pro-inflammatory cytokines, including IFN-gamma, and were recently shown to play an important role in IBD pathogenesis. In this new study, a team of researchers at Beth Israel Deaconess Medical Center (BIDMC) continued their previous studies on an enzyme called CD39, a highly represented ectonucleotidase in immune cells. The function of CD39 as an ecto-enzyme is to cleave extracellular ATP and ADP (both potent activators of immune cells) into AMP, and then convert to adenosine, an immunosuppressive molecule, as Simon C. Robson, MB, ChB, PhD, Chief of the Division of Gastroenterology at BIDMC and Charlotte F. and Irving W. Rabb Professor of Medicine at Harvard Medical School explained in a
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