H2AX参与白血病细胞诱导NK细胞凋亡的研究

摘要

Objective To discuss the possible mechanism of H2AX involved in the NK cells apoptosis induced by leukemia cells K562. Methods NK92 cells cultured in vitro with Fas-activated antibody CH11, the NK cells apoptosis detected by flow cytometry; during NK cell apoptosis, H2AX phosphorylation also detected. Results As the concentration of CHI 1 (0, 2. 5, 5, 10, 20) μg/ml increased, cell apoptosis was significantly increased in a dose-dependent manner, similarly; suggested that CH11 induced apoptosis of NK cells in a dose-dependent manner; Additionally, the phosphorylation level of H2AX also increased gradually with the concentration of CH11 (0, 5, 10, 40, 80 μg/ml), and in a dose dependent manner, disclosed that phosphorylation of H2AX involved in the apoptosis. Conclusion Phosphorylation of H2AX participates in the process of apoptosis of NK-92 cells induced by leukemic cells.%目的 初步探讨H2AX磷酸化水平是否参与白血病细胞系诱导自然杀伤(NK)细胞凋亡.方法 体外培养 NK92细胞,利用Fas激活性抗体CH11作用于NK92细胞,用流式细胞术检测NK92细胞的凋亡情况;检测NK92细胞凋亡的同时用流式细胞学技术检测H2AX磷酸化的水平.结果 随着CH11浓度(0、2.5、5、10、20 μg/ml)的升高, NK92细胞凋亡现象明显增加,并呈剂量依赖性,表明NK细胞凋亡随着CH11浓度的升高而增加;同时H2AX的磷酸化水平也随CH11浓度(0、5、10、40、80 μg/ml)逐步增高,并呈剂量依赖性,提示H2AX的磷酸化作用参与细胞凋亡过程,并且随浓度的增加而增加.结论 H2AX的磷酸化作用参与白血病细胞诱导NK细胞的凋亡过程.