Article abstract
Nature Immunology 10, 603 - 609 (2009)
Published online: 17 May 2009 | doi:10.1038/ni.1736
A protective function for interleukin 17A in T cell–mediated intestinal inflammation
William O'Connor Jr1, Masahito Kamanaka1, Carmen J Booth2, Terrence Town1,6, Susumu Nakae3, Yoichiro Iwakura3, Jay K Kolls4 & Richard A Flavell1,5
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.
- Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA.
- Section of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut, USA.
- Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan.
- Children's Hospital of Pittsburgh, Pittsburgh, Pennsylvania, USA.
- Howard Hughes Medical Institute, Yale University, New Haven, Connecticut, USA.
- Present address: Department of Neurosurgery, Biomedical Sciences and Department of Medicine, Maxine Dunitz Neurosurgical Institute Cedars-Sinai Medical Center, Los Angeles, California, USA.
Correspondence to: Richard A Flavell1,5 e-mail: richard.flavell@yale.edu
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