Invariant Vα19i T cells regulate autoimmune inflammation
Invariant Vα19i T cells regulate autoimmune inflammation
复制标题
DOI：
10.1038/ni1370
复制
发表时间：
2006-09-01
影响因子：
30.5
通讯作者：
Yamamura, Takashi
中科院分区：
文献类型：
--
作者：
Croxford, J. Ludovic;Miyake, Sachiko;Yamamura, Takashi
表达不变的V(α)19-J(α)33T细胞受体α链(V(α)19i TCR)的T细胞受非多态的主要组织相容性复合体Ib类分子MR1的限制。V(Alpha)19iT细胞是否参与自身免疫尚不清楚。在这里，我们证明了表达V(α)19i TCR转基因的T细胞抑制了实验性自身免疫性脑脊髓炎(EAE)的诱导和进展，EAE是多发性硬化症的小鼠模型。同样，在缺乏V(α)19i T细胞的MR1缺陷小鼠中，EAE加重。IL-10的产生至少部分是通过ICOS共刺激分子介导的B细胞与V(α)19i T细胞之间的相互作用来实现的。这些结果提示V(α)19iT细胞具有免疫调节功能。
T cells expressing an invariant V(alpha)19-J(alpha)33 T cell receptor alpha-chain (V(alpha)19i TCR) are restricted by the nonpolymorphic major histocompatibility complex class Ib molecule MR1. Whether V(alpha)19i T cells are involved in autoimmunity is not understood. Here we demonstrate that T cells expressing the V(alpha)19i TCR transgene inhibited the induction and progression of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis. Similarly, EAE was exacerbated in MR1-deficient mice, which lack V(alpha)19i T cells. EAE suppression was accompanied by reduced production of inflammatory mediators and increased secretion of interleukin 10. Interleukin 10 production occurred at least in part through interactions between B cells and V(alpha)19i T cells mediated by the ICOS costimulatory molecule. These results suggest an immunoregulatory function for V(alpha)19i T cells.