Department of Immunology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH 44195, USA.
J Immunol. 2011 Apr 15;186(8):4546-50. doi: 10.4049/jimmunol.1004021. Epub 2011 Mar 14.
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.
Th17 细胞被认为与结肠炎的发病机制有关；然而，体内致结肠炎的 Th17 免疫产生的细胞机制仍不清楚。在这项研究中，我们报告说，IL-17(+)γδ T 细胞的一个亚群在增强体内 Th17 分化和 T 细胞介导的结肠炎中起着关键作用。TCRβ(-/-) 小鼠对 T 细胞介导的结肠炎高度敏感，而 TCRβδ(-/-) 小鼠则对该疾病具有抗性。重要的是，与 CD4 T 细胞共转移 IL-17(+)但不是 IL-17(-)γδ T 细胞足以增强 Th17 分化并在 TCRβδ(-/-)受者中诱导完全性结肠炎。总之，我们的结果提供了 IL-17(+)γδ T 细胞亚群在支持体内 Th17 分化和可能促进肠道炎症发展中的新功能。
