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作 者:邵晓轶[1,2] 路丽明[1] 周芸[1] 马妍慧[1] 杨志强[1] 顾鹏[1] 周光炎[1]
机构地区:[1]上海交通大学医学院上海市免疫学研究所,上海200025 [2]南通大学医学院免疫学系
出 处:《南通大学学报(医学版)》2012年第5期333-337,330,共5页Journal of Nantong University(Medical sciences)
基 金:国家自然科学基金资助项目(30772018;30972691);南通市科技计划项目(BK2011019);江苏高校优势学科建设工程资助项目
摘 要: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.
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