Laboratory of Developmental Immunology and CREST Program of Japan Science and Technology Agency, Graduate School of Frontier Biosciences, Graduate School of Medicine and WPI Immunology Frontier Research Center, Osaka University, Osaka, 565-0871, Japan.
Int Immunol. 2010 Feb;22(2):129-39. doi: 10.1093/intimm/dxp119. Epub 2009 Dec 30.
Although recent studies have identified regulatory roles for Foxp3(+)CD8(+) T cells, the mechanisms that induce their development and underlie their functions in vivo have not been elucidated. Here, we show that IL-6 positively regulates the Foxp3(+)CD8(+) T-cell development and function. The Foxp3(+)CD8(+) T cells that differentiated in vitro in the presence of IL-6 suppressed autoimmune colitis and arthritis in vivo. Moreover, Foxp3(+)CD8(+) T cells that developed in vivo in the presence of enhanced IL-6 signaling suppressed the development of a spontaneous T(h)17 cell-mediated autoimmune arthritis. Thus, we concluded that Foxp3(+)CD8(+) T cells develop in response to IL-6 and regulate chronic inflammation in T(h)17 cell-mediated F759 autoimmune arthritis. These results suggested that Foxp3(+)CD8(+) T cells may develop in response to IL-6 under certain inflammatory conditions in vivo and may regulate some other chronic inflammation diseases.
虽然最近的研究已经确定了 Foxp3(+)CD8(+)T 细胞的调节作用，但诱导其发育并阐明其在体内功能的机制尚未阐明。在这里，我们表明 IL-6 可正向调节 Foxp3(+)CD8(+)T 细胞的发育和功能。体外在 IL-6 存在的情况下分化的 Foxp3(+)CD8(+)T 细胞在体内抑制自身免疫性结肠炎和关节炎。此外，体内在增强的 IL-6 信号存在的情况下发育的 Foxp3(+)CD8(+)T 细胞抑制了自发性 T(h)17 细胞介导的自身免疫性关节炎的发展。因此，我们得出结论，Foxp3(+)CD8(+)T 细胞是响应 IL-6 而发育的，并调节 T(h)17 细胞介导的 F759 自身免疫性关节炎中的慢性炎症。这些结果表明，Foxp3(+)CD8(+)T 细胞可能会在体内某些炎症条件下响应 IL-6 而发育，并可能调节其他一些慢性炎症疾病。
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