小鼠膜型B7-H1分子激活同种异体Tr1细胞介导免疫抑制

Membranous B7-H1 molecule activates allogenic Tr1 cells and mediates immunosuppression in mice

目的:观察小鼠膜型B7-H1分子对同种异体CD4+T细胞分化和功能的影响,探讨B7-H1诱导免疫抑制的作用机制。方法:用经稳定转染而高表达膜型B7-H1分子的小鼠1B4.B6细胞刺激同种异体小鼠初始CD4+T细胞,检测被激活的CD4+T细胞的细胞因子分泌格局、免疫功能及Foxp3的表达。结果:与转染空载体的对照细胞相比,高表达B7-H1的1B4.B6细胞刺激同种异体CD4+T细胞产生高水平白细胞介素10(interleukin 10,IL-10)和干扰素γ(interferonγ,IFN-γ)、极低水平IL-4和IL-2。活化的CD4+T细胞具有免疫抑制活性,不表达Foxp3。结论:稳定转染B7-H1的1B4.B6细胞可通过其表面高表达的B7-H1分子诱导同种异体Ⅰ型调节性T细胞(type 1 regulatory T cells,Tr1)的分化。

Objective： To determine the influences of mouse membranous B7-H1 molecule on the differentiation and function of allogenic CD4＋T cells,and to explore the mechanism of B7-H1 acting as an immunosuppressive factor.Methods： B7-H1-transfected 1B4.B6 cell line and mock-transfected control were used to stimulate allogenic nave CD4＋T cells respectively,and the cytokines secretion,immune funciton and Foxp3 expression of the activated CD4＋T cells were examined.Results： Compared with the mock-transfected control,the B7-H1-transfected 1B4.B6 cells induced the allogenic CD4＋T cells to produce high levels of IL-10 and IFN-γ and a very low level of IL-4 and IL-2.The activated CD4＋T cells didn＇t express the transcription factor Foxp3,and played immunosuppressive roles in vitro.Conclusion： B7-H1-transfected 1B4.B6 cells induce the generation of Tr1 cells via high expression of membranous B7-H1.