| Literature DB >> 21402889 |
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.Entities:
Mesh:
Substances:
Year: 2011 PMID: 21402889 PMCID: PMC3200541 DOI: 10.4049/jimmunol.1004021
Source DB: PubMed Journal: J Immunol ISSN: 0022-1767 Impact factor: 5.422