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Nat Immunol. 2009 Jun;10(6):603-9. doi: 10.1038/ni.1736.

A protective function for interleukin 17A in T cell-mediated intestinal inflammation.

Author information

1
Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.

Abstract

Interleukin 23 (IL-23) and IL-17 have been linked to the pathogenesis of several chronic inflammatory disorders, including inflammatory bowel disease. Yet as an important function for IL-23 is emerging, the function of IL-17 in inflammatory bowel disease remains unclear. Here we demonstrate IL-17A-mediated protection in the CD45RBhi transfer model of colitis. An accelerated wasting disease elicited by T cells deficient in IL-17A correlated with higher expression of genes encoding T helper type 1-type cytokines in colon tissue. IL-17A also modulated T helper type 1 polarization in vitro. Furthermore, T cells deficient in the IL-17 receptor elicited an accelerated, aggressive wasting disease relative to that elicited by wild-type T cells in recipient mice. Our data demonstrate a protective function for IL-17 and identify T cells as not only the source but also a target of IL-17 in vivo.

PMID:
19448631
PMCID:
PMC2709990
DOI:
10.1038/ni.1736
[Indexed for MEDLINE]
Free PMC Article

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