Tracking the Role of Immune Cells in IBD

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As many as 1.6 million Americans have Inflammatory Bowel Disease, a chronic inflammation of the digestive tract that most commonly manifests as Crohn’s disease (CD) or ulcerative colitis (UC). Determining why some people develop the disease has been at the forefront of IBD research. New research on small protein cells called cytokines may hold the key to identifying factors that lead to the development of Inflammatory Bowel Disease.

Cytokines help the immune system communicate during an immune response. The body releases cytokines into circulation or directly into tissue to interact with immune cells. Overproduction of these cells can result in inflammatory conditions like arthritis and IBD.

Current research is looking at the specific cytokine IL-36γ. IL-36γ appears to work in two ways to control whether the immune system promotes or suppresses IBD development. According to a press release by Georgia State researchers, IL-36γ increases inflammation by promoting the development of a specific type of Th9.

This Th9 cell is a T-helper cell that promotes inflammation in IBD. The research, published in Mucosal Immunology, also found that the same cells inhibit the T cells known as T-reg cells, which suppress the development of IBD. By both increasing inflammation and preventing cells from suppressing IBD, the cytokine IL-36γ may play a critical role in helping researchers understand why IBD develops in some people and not in others.

In the future, research will look into ways to block the action of IL-36γ in people who have IBD. If this can be achieved, it might well prove a very promising treatment for the millions of people around the globe who live with this painful disease.

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