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Study provides new clues to IBD therapy

View:215 Time:2017-04-19

A recent study published 22 March 2017 in the journal Mucosal Immunity has revealed that a specific cytokine controls whether immune cells promote or inhibit inflammatory bowel disease (IBD). The study is led by Tim Denning from the Institute for Biomedical Sciences at Georgia State.

IBD, represented mainly ulcerative colitis and Crohn's disease, is a chronic condition that involves inflammation in the gut. According to estimates, IBD affects approximately 1.5 million people in the United States and more than 250,000 in the UK. Its incidence is increasing worldwide for unknown reasons. For example, IBD cases among children under five have increased 7.2% per year between 1999 to 2010.

The etiology of IBD remains unclear, but it is thought that IBD results from the interaction of environment and genetic factors leading to immune responses and inflammation in the gut.

In this work, Denning and colleagues found that a member of the interleukin 1 cytokine family, IL-36γ, controls whether T cells become aggressive or suppressive. Specifically, IL-36γ potently inhibits regulatory T cell (Treg) development, while promoting the differentiation of T helper 9 (Th9) cells.

Treg cells are immunosuppressive and generally suppress both physiological and pathological immune responses. Previous studies have shown that Treg cells suppress IBD and a deficiency in these cells is involved in IBD pathogenesis. Th9 cells have pro-inflammatory capacity. These cells can aid in immune responses against diseases and infections, but can also contribute to the development of certain diseases including IBD, asthma, allergy, and cancer.

The finding that IL-36γ inhibits the development of Treg cells and drives the differentiation of Th9 cells reveals that IL-36γ plays a key role in regulating Treg-Th9 cell balance. It is well-established that the intestinal immune system must strike the right balance between pro-inflammatory and anti-inflammatory responses, because disruptions in this balance may cause IBD. So the identification of IL-36γ as a regulator of Treg-Th9 cell balance is of great importance.

In summary, the study suggests that drugs that target the protein IL-36γ might be used as therapeutic agents for IBD, but more experimental investigation is needed to further explore the function of IL-36γ in the disease.

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