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目的 探讨CD2 8协同结核杆菌 (M .tb)低分子多肽激活人外周血γδ+ T细胞时 ,其胞内信号的传递经过磷酸肌醇 3激酶 (PI3K)的介导作用。方法 用激发型抗CD2 8单抗模拟第二信号 ,与M .tb抗原一起刺激纯化的T细胞 ,同时用特异性PI3K抑制剂LY2 940 0 2阻断PI3K的活性 ,用流式细胞仪分析γδ+ T细胞上CD6 9分子的表达及γδ+ T细胞的增殖效应。结果 随着LY2 940 0 2浓度的增加 ,γδ+ T细胞表面CD6 9分子的表达率降低 ,其增殖效应亦被不同程度地阻断。结论 抗CD2 8单抗可协同M .tb抗原激活γδ+ T细胞 ,其活化信号在γδ+ T细胞内的转导经过PI3K的介导。
OBJECTIVE: To investigate the effect of phosphoinositide 3 kinase (PI3K) on the intracellular signal transduction of CD8 + Mycobacterium tuberculosis (M.tb) low-molecular-weight peptide in human peripheral blood γδ + T cells. Methods The second signal was stimulated by the stimulated anti-CD28 mAb and the purified T cells were stimulated with the M tb antigen. At the same time, the PI3K activity was blocked by the specific PI3K inhibitor LY2 940 0 2, and analyzed by flow cytometry + T cells and the effect of γδ + T cell proliferation. Results As the concentration of LY2 940 02 increased, the expression of CD6 9 on γδ + T cells decreased, and the proliferative effects of γ6 + T cells were also blocked to some extent. Conclusion Anti-CD8 mAb can activate γδ + T cells in combination with M.tb antigen, and its activation signal is mediated by PI3K in γδ + T cells.