AGEs对胰腺癌细胞株表面PD-L1表达的影响及生物学意义

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。

Effect of advanced glycosylation end products on PD-L1 expression of human pancreatic cancer cells and its biological significance

Objective To investigate the effect of advanced glycosylation end products(AGEs) on programmed death-1 ligand 1(PD-L1) expression of human pancreatic cancer cell line Patu8988 and the effect of AGEs-induced tumor on the proliferation of T cells. Methods Patu8988 in test group was treated with AGE-bovine serum albumin (AGE-BSA) for 72 h,and BSA was used in control group.The expression of PD-L1 was detected by flow cytometry.The proliferation of T cells was measured by cell counting kit-8(CCK-8) assay after co-cultured with Patu8988 cell line pre-treated with AGE-BSA for 72 h. Results Compared with control group,the expression of PD-L1 after treated with AGE-BSA was increased in a dose-dependent manner(P<0.05).The proliferation of T cells in co-cultivation with Patu8988 cells pre-treated with AGEs was inhibited(P<0.05), which could be reversed by anti-PD-L1 monoclonal antibody(P<0.05). Conclusion AGEs can suppress the proliferation of T cells by up-regulating PD-L1 expression on Patu8988 cell line.