Literature DB >> 21402889

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

Jeong-su Do1, Anabelle Visperas, Chen Dong, William M Baldwin, Booki Min.   

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(+) 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.

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Year:  2011        PMID: 21402889      PMCID: PMC3200541          DOI: 10.4049/jimmunol.1004021

Source DB:  PubMed          Journal:  J Immunol        ISSN: 0022-1767            Impact factor:   5.422


  27 in total

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Review 4.  Cytokine crowdsourcing: multicellular production of TH17-associated cytokines.

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10.  Cutting edge: IFN-γR signaling in non-T cell targets regulates T cell-mediated intestinal inflammation through multiple mechanisms.

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