Individuals with inflammatory bowel diseases (IBDs) experience episodes of inflammation in their gut that can cause abdominal pain, vomiting, and diarrhea, among other things.
Exactly what causes IBD has not been determined but it is now considered to involve inappropriate over activation of the immune system in the gut, and the proinflammatory factor IL-6 is thought to have a crucial role in this.
New insight into the molecular mechanisms controlling IL-6 production in a mouse model of IBDs has now been provided by Markus Neurath and colleagues, at the University of Mainz, Germany, and might lead to the development of new drugs to treat individuals with IBDs.
Initial analysis indicated that a molecule known as IRF4, which regulates several functions in immune cells known as T cells, was expressed at higher levels in T cells in the gut of individuals with IBDs than in the gut of healthy individuals.
Consistent with increased IRF4 having an important role in the development of IBD, T cells from mice lacking IRF4 did not cause intestinal inflammation when transplanted into immunodeficient mice, whereas normal T cells did. Further, IRF4-deficient mice were protected from intestinal inflammation in two other models of IBD, and this protection was overcome by the administration of IL-6 to the mice.
The authors therefore conclude that IRF4 is a crucial regulator of IL-6 production in the intestine and that targeting IRF4 might provide a new approach to treating individuals with IBDs.
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