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目的:探讨B7-H1阻断对CD3AK细胞增殖活化及其抗肿瘤免疫效应的影响。方法:利用CD3单克隆抗体(mAb)刺激健康人外周血淋巴细胞诱导产生CD3AK细胞,然后利用B7-H1阻断型抗体阻断B7-H1通路,3H-TdR渗入法检测阻断后CD3AK细胞的增殖能力,ELISA法检测阻断后CD3AK细胞分泌IFN-γ、TNF-α和IL-10的水平,同时将CD3AK细胞作用于膀胱肿瘤BIU-87细胞,MTT法检测阻断后CD3AK细胞的杀伤活性。结果:B7-H1阻断后,CD3AK细胞的增殖能力明显增强,体外存活时间明显延长;其分泌IFN-γ、TNF-α的水平明显提高,而分泌IL-10的水平明显下降;同时CD3AK细胞对BIU-87细胞的杀伤活性亦明显升高。结论:阻断B7-H1通路可以促进和维持CD3AK细胞的增殖和活化,并增强其抗肿瘤的免疫效应。阻断B7-H1通路将有望成为肿瘤免疫治疗的新策略。
Objective: To investigate the effect of B7-H1 block on the proliferation and activation of CD3AK cells and its antitumor immunity. Methods: CD3AK cells were induced by CD3 monoclonal antibody (mAb) in peripheral blood of healthy volunteers. Then the B7-H1 blocking antibody was used to block the B7-H1 pathway. 3H-TdR infiltration was used to detect the expression of CD3AK Proliferative ability and the level of IFN-γ, TNF-α and IL-10 secreted by CD3AK cells were detected by ELISA. Meanwhile, CD3AK cells were treated with BIU-87 cells. The killing activity of CD3AK cells was detected by MTT assay . Results: After B7-H1 was blocked, the proliferation of CD3AK cells was significantly enhanced and the survival time in vitro was significantly prolonged. The levels of IFN-γ and TNF-α secreted by B7-H1 were significantly increased, while the levels of IL-10 secreted by CD3AK cells were significantly decreased. BIU-87 cell killing activity was also significantly increased. Conclusion: Blocking the B7-H1 pathway can promote and maintain the proliferation and activation of CD3AK cells and enhance its anti-tumor immune effect. Blocking the B7-H1 pathway is expected to be a new strategy for tumor immunotherapy.