Interleukin 17 (IL-17)-a soluble factor thought to promote inflammation and autoimmunity-can actually suppress the onset of inflammatory bowel disease, shows a paper published online in this week’s Nature Immunology.
Previous work documented high concentrations of IL-17 and interferon-gamma, another cytokine implicated in inflammation and autoimmunity, in colon tissue of humans with Crohn’s disease and mice with colitis.
Using a mouse model of colitis in which immune cells called T cells initiate disease, Richard Flavell and colleagues note that T cells lacking IL-17 or the IL-17 receptor induced more severe colitis than T cells able to produce and respond to IL-17. IL-17-deficient T cells also released more interferon-gamma.
These findings suggest net effects of IL-17 may be pro- or anti-inflammatory, and likely depend on the tissue and environment being examined.