Objective: To investigate the effect of chidamide on the killing activity of NK (Natural killer cell, NK) cells targeting K562 cells and its related mechanism.
Methods: K562 cells were pretreated with chidamide at different concentrations and cocultured with NK cells at different effect-target ratios. The killing effect of chidamide on K562 cells by NK cells, the expression of natural killer group 2 member D (NKG2D) ligands and apoptosis rate of K562 cells were detected by flow cytometry.
Results: The killing sensitivity of NK cells to K562 cells could be enhanced by chidamide. The expression of ULBP2 on K562 cell surface could be up-regulate, however, the expression of ULBP1 and MICA/MICB showed no statistically difference as compared with control group. Chidamide showed no obvious cytotoxicity to K562 cells.
Conclusion: Chidamide can significantly improve killing efficiency of NK cells on K562 cells, which may be related to the up-regulation of ULBP2 expression.
题目: 西达本胺对NK细胞体外杀伤K562细胞活性的影响及其相关机制.
目的: 观察西达本胺对自然杀伤细胞（NK）体外杀伤K562细胞活性的影响并探讨其作用机制.
方法: 用不同浓度的西达本胺预处理K562细胞，与NK细胞不同效靶比共同孵育，采用流式细胞术检测西达本胺作用于K562细胞后NK细胞对其杀伤作用、K562细胞表面NKG2D相关配体表达量及K562细胞凋亡率的变化.
结果: 西达本胺可增加K562细胞对NK细胞杀伤的敏感性，同时可上调K562细胞表面ULBP2表达，对ULBP1、MICA/MICB表达无明显影响，西达本胺于K562细胞本身无明显细胞毒性作用.
结论: 西达本胺可能通过增加ULBP2的表达提高K562细胞对NK细胞杀伤敏感性.