Ulcerative colitis (UC) and Crohn’s disease are marked by runaway inflammation in the gut that permanently damages the intestines, but why inflammation becomes excessive in patients with these conditions is unclear. A new study led by researchers from the University of Texas (UT) Southwestern, published online on May 18, 2020 in Nature Immunology, offers clues to the mechanism behind this phenomenon, providing several new potential targets to treat these often devastating conditions. The article is titled “Deubiquitination of NLRP6 Inflammasome by Cyld Critically Regulates Intestinal Inflammation.” Approximatley 1.6 million Americans suffer from these and other inflammatory bowel diseases (IBDs). While a variety of medications are used to treat these conditions, including corticosteroids, immunomodulators, and biologics, up to a third of patients do not respond to these drugs, and the medications often lose efficacy over time for those who do respond, says Venuprasad Poojary (photo) (https://profiles.utsouthwestern.edu/profile/189208/venuprasad-poojary.html), PhD, Associate Professor of Internal Medicine and Immunology at UTSW. New medications are urgently needed to help patients avoid invasive treatments such as surgeries. But efforts to develop pharmaceuticals for these conditions have been stymied because the mechanisms behind chronic gastrointestinal inflammation aren’t well understood, Dr. Poojary says. To help flesh out this mechanism, Dr. Poojary and his colleagues started by focusing on a single gene called Cyld, which previous studies have shown is often mutated in patients with various IBDs.
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