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Cutting edge: Generation of colitogenic Th17 CD4 T cells is enhanced by IL-17+ ?? T cells.


ABSTRACT: 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(+) ?? T cells plays a crucial role in enhancing in vivo Th17 differentiation and T cell-mediated colitis. TCR?(-/-) mice were highly susceptible to T cell-mediated colitis, whereas TCR??(-/-) mice were resistant to the disease. Importantly, cotransfer of IL-17(+) but not of IL-17(-) ?? T cells with CD4 T cells was sufficient to enhance Th17 differentiation and induce full-blown colitis in TCR??(-/-) recipients. Collectively, our results provide a novel function of IL-17(+) ?? T cell subsets in supporting in vivo Th17 differentiation and possibly in fostering the development of intestinal inflammation.

SUBMITTER: Do JS 

PROVIDER: S-EPMC3200541 | biostudies-literature | 2011 Apr

REPOSITORIES: biostudies-literature

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Cutting edge: Generation of colitogenic Th17 CD4 T cells is enhanced by IL-17+ γδ T cells.

Do Jeong-su JS   Visperas Anabelle A   Dong Chen C   Baldwin William M WM   Min Booki B  

Journal of immunology (Baltimore, Md. : 1950) 20110314 8


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 c  ...[more]

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