Th 17 cells have been implicated in the pathogenesis of colitis; however, a cellular mechanism by which colitogenic Th17 immunity arises in vivo remains unclear. In this study, we report that a subset of IL-17+ γδ T cells plays a crucial role in enhancing in vivo Th17 differentiation and T cell-mediated colitis. TCRβ-/- mice were highly susceptible to T cell-mediated colitis, whereas TCRβδ -/- mice were resistant to the disease. Importantly, cotransfer of IL-17+ but not of IL-17- γδ T cells with CD4 T cells was sufficient to enhance Th17 differentiation and induce full-blown colitis in TCRβδ-/- recipients. Collectively, our results provide a novel function of IL-17+ γδ T cell subsets in supporting in vivo Th17 differentiation and possibly in fostering the development of intestinal inflammation.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Immunology|
|State||Published - Apr 15 2011|
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