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目的探索结核分枝杆菌Rv2986c蛋白诱导小鼠树突状细胞成熟及Na?ve CD4~+T细胞极化的作用。方法克隆表达Rv2986c蛋白,用纯化后的蛋白刺激小鼠树突状细胞,流式检测树突状细胞MHC-Ⅱ表面分子,ELISA检测培养上清中IL-6和IL-12p40分泌情况。将Na?ve CD4~+T细胞与经Rv2986c刺激后的树突状细胞共培养,检测培养上清中IFN-γ的分泌水平。结果成功克隆表达了Rv2986c蛋白。经Rv2986c蛋白刺激后,树突状细胞MHC-Ⅱ表面分子表达水平显著增高,IL-6和IL-12p40释放水平显著升高。淋巴细胞共培养上清液中IFN-γ分泌量显著增加。结论结核分枝杆菌蛋白Rv2986c能促进小鼠树突状细胞成熟,激活抗原递呈作用,诱导CD4~+T向Th1型极化。
Objective To explore the role of Mycobacterium tuberculosis Rv2986c protein in the induction of mouse dendritic cell maturation and Na? Ve CD4 ~ + T cell polarization. Methods Rv2986c protein was cloned and expressed. The dendritic cells were stimulated with the purified protein. The surface molecules of dendritic cells were detected by flow cytometry. The secretion of IL-6 and IL-12p40 in the culture supernatants was detected by ELISA. Na? Ve CD4 ~ + T cells were co-cultured with dendritic cells stimulated with Rv2986c to detect the secretion of IFN-γ in the culture supernatant. Results The Rv2986c protein was successfully cloned and expressed. Rv2986c protein stimulation, dendritic cells MHC-Ⅱ surface molecule expression was significantly increased, IL-6 and IL-12p40 release was significantly increased. IFN-γ secretion in lymphocyte co-culture supernatants significantly increased. Conclusion Mycobacterium tuberculosis protein Rv2986c can promote the maturation of dendritic cells in mice, activate the antigen presentation and induce the CD4 ~ + T to Th1 type polarization.