Key Protein May Lead to Novel IBD Therapies for Colon Inflammation, Crohn’s, Ulcerative Colitis

Key Protein May Lead to Novel IBD Therapies for Colon Inflammation, Crohn’s, Ulcerative Colitis
Researchers identified a novel cellular mechanism responsible for increasing inflammation in the colon (large intestine), a common feature triggering Crohn’s disease, ulcerative colitis, even colon cancer. The study, “Itch inhibits IL-17-mediated colon inflammation and tumorigenesis by ROR-γt ubiquitination,” was recently published in the journal Nature Immunology, and identified novel players for future targeted therapeutics in inflammatory bowel diseases (IBDs) and colon cancer. Researchers at Baylor Institute for Immunology Research, part of Baylor Scott & White Research Institute, investigated the role of an ubiquitin ligase protein, referred to as Itch, in inflamed colons. While inflammation is a natural response to halt microbial infection and tissue injury, when uncontrolled it can bring on the opposite effect and damage the colon tissue. This is a major risk factor for the development and growth of colon cancer. Previous studies showed that dysregulated secretion of a pro-inflammatory interleukin -- interleukins are a subset of a larger group of cellular messenger molecules called cytokines, which mediate important responses in cells -- called interleukin 17 (IL-17), by cells within the colon is associated with colon inflammation and cancer. However, the cell-intrinsic molecular mechanisms regulating IL-17 remained unknown. “We found that deficiency in the Itch protein led to spontaneous colitis and increased susceptibility to colon cancer. O
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