Journal
JOURNAL OF IMMUNOLOGY
Volume 186, Issue 8, Pages 4546-4550Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1004021
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- National Institutes of Health [AI074932]
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Th 17 cells have been implicated in the pathogenesis of colitis; however, a cellular mechanism by which colito-genic Th17 immunity arises in vivo remains unclear. In this study, we report that a subset of IL-17(+) gamma delta T cells plays a crucial role in enhancing in vivo Th17 differentiation and T cell-mediated colitis. TCR beta(-/-) mice were highly susceptible to T cell-mediated colitis, whereas TCR beta delta(-/-) mice were resistant to the disease. Importantly, cotransfer of IL-17(+) but not of IL-17(-) gamma delta T cells with CD4 T cells was sufficient to enhance Th17 differentiation and induce full-blown colitis in TCR beta delta(-/-) recipients. Collectively, our results provide a novel function of IL-17(+) gamma delta T cell subsets in supporting in vivo Th17 differentiation and possibly in fostering the development of intestinal inflammation. The Journal of Immunology, 2011, 186: 4546-4550.
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