Intestinal Goings-On

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Science  30 Apr 2010:
Vol. 328, Issue 5978, pp. 548-549
DOI: 10.1126/science.328.5978.548-c

Allelic variants in the human interleukin-23 (IL-23) receptor are associated with susceptibility to several inflammatory diseases, such as psoriasis and inflammatory bowel disease. In mice, both T cell–dependent and T cell–independent “innate” models of colitis are driven by IL-23–mediated inflammation. In T cell–dependent models, IL-23–dependent inflammation is primarily the result of pro-inflammatory cytokine production by CD4+ T helper type 17 (TH17) cells. The mechanistic basis for IL-23–driven innate colitis has not been determined.

Buonocore et al. show that, in a manner similar to that of T cell–dependent colitis, innate colitis is also driven by TH17-associated pro-inflammatory cytokines. Rather than being produced by T cells, however, these cytokines are produced by a population of IL-23–responsive colonic lamina propria cells. These cells are similar in phenotype to lymphoid tissue inducer–like cells, which have previously been shown to produce TH17-associated cytokines. Depletion of these cells led to abrogation of colitis, and the authors were able to confirm their results in another mouse model of innate colitis. These results suggest that the TH17 gene expression profile is an important driver of intestinal inflammation in both the innate and adaptive immune systems.

Nature 10.1038/nature08949 (2010).

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