A New Target for Inflammatory Bowel Disease to Aid in Treatment?

Cytokine IL-36 Gamma Controls Immune Cell Function Associated with IBD, Particularly in Ulcerative Colitis

A study led by researchers from Georgia State University, in collaboration with colleagues from Emory University and University of Michigan, reports that the regulation of inflammatory bowel disease (IBD) by immune cells can be affected by a specific cytokine or small protein. Cytokine IL-36γ was found to induce the development of the T helper cell Th9, which is associated with IBD and other conditions. Additionally, IL-36γ was found to suppress the population of regulatory T cells, or Tregs, which have been shown to inhibit IBD. Lead author Tim Denning, PhD, commented, “Our conclusions were that IL-36γ plays a critical role in driving the differentiation of proinflammatory Th9 cells and inhibiting the development of the suppressive Tregs. We think this can have major implications in the treatment of human inflammatory bowel disease, particularly ulcerative colitis, which has been shown to be associated with Th9 cells.” The findings are published in the journal Mucosal Immunology.

IBD, the 2 main types of which are Crohn’s disease and ulcerative colitis, affects some 1.5 million people in the US, causing pain, fatigue, severe diarrhea, and weight loss. Building on prior work that found high levels of IL-36γ in inflamed intestines in both mice and humans, the present research sought to further illuminate the association of IL-36γ to IBD. Future work will focus on possible means to block the ability of IL-36γ to its receptor, potentially opening new treatment avenues for patients with IBD.

Read a news story about the findings.

Read the journal abstract.

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