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目的研究糖基化终产物(AGEs)对人胰腺癌细胞株Patu8988表面程序性死亡配体1(PD-L1)表达的影响,探讨AGEs诱导的肿瘤细胞对T细胞增殖的作用。方法以糖基化牛血清白蛋白(AGE-BSA)干预细胞株Patu8988为实验组,以牛血清白蛋白(BSA)为对照组,孵育72h后用流式细胞术分析各组细胞表面PD-L1表达的变化;AGE-BSA诱导的Patu8988细胞与人T细胞共培养,72h后用细胞增殖和细胞计数试剂盒8(CCK-8)检测T细胞增殖。结果 AGE-BSA诱导72h后,Patu8988细胞表面PD-L1的表达呈浓度依赖性升高(P<0.05)。肿瘤细胞经AGEs诱导后抑制T细胞增殖能力增强(P<0.05),用抗PD-L1单抗阻断后抑制作用减弱(P<0.05)。结论 AGEs通过上调Patu8988细胞表面PD-L1的表达抑制T细胞增殖。
Objective To investigate the effect of advanced glycation end products (AGEs) on the expression of PD-L1 on human pancreatic cancer cell line Patu8988 and to explore the effect of AGEs on the proliferation of T cells. Methods The cell line Patu8988 with glycosylated bovine serum albumin (AGE-BSA) was used as the experimental group and the bovine serum albumin (BSA) as the control group. After incubation for 72 hours, the cell surface PD-L1 The changes of the expression of AGE-BSA were observed. Patu8988 cells induced by AGE-BSA were co-cultured with human T cells. T cell proliferation was detected by Cell Proliferation and Cell Counting Kit 8 (CCK-8) 72h later. Results The expression of PD-L1 on Patu8988 cells induced by AGE-BSA increased in a concentration-dependent manner (P <0.05). The ability of tumor cells to inhibit T cell proliferation induced by AGEs was enhanced (P <0.05), and the inhibition by anti-PD-L1 mAb was weakened (P <0.05). Conclusion AGEs can inhibit the proliferation of T cells by up-regulating the expression of PD-L1 on the surface of Patu8988 cells.