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首页|期刊导航|中国耳鼻咽喉头颈外科|S-烯丙基巯基半胱氨酸促进CD8+T细胞杀伤功能的机制研究

S-烯丙基巯基半胱氨酸促进CD8+T细胞杀伤功能的机制研究OA北大核心CSTPCD

Mechanism study on S-allylmercaptocysteine promoting CD8+T cell killing function

中文摘要英文摘要

目的 探究S-烯丙基巯基半胱氨酸(S-allylmercaptocysteine,SAMC)对CD8+T细胞杀伤鼻咽癌细胞功能的影响及机制.方法 将人鼻咽癌细胞HK-1和C666-1与SAMC共培养,分为0、25、50、100 μmol/L SAMC组,Western blot检测肿瘤细胞程序性死亡配体-1(programmed cell death-ligand 1,PD-L1)表达.CD8+T细胞分别与HK-1和C666-1细胞以10∶1的比例共培养并加入0、25、50、100 μmol/L SAMC,检测CD8+T对HK-1和C666-1的杀伤能力,酶联免疫法(ELISA)检测干扰素(INF-γ)和肿瘤坏死因子-α(TNF-α)浓度,构建鼻咽细胞HK-1的小鼠皮下移植瘤模型,分为对照组、CD8+T细胞组、SAMC组、SAMC+CD8+T细胞组,各组小鼠治疗期间测量瘤体积,治疗结束后取小鼠肿瘤组织,Western blot检测肿瘤组织中PD-L1表达,ELISA检测小鼠血清INF-γ和TNF-α浓度.结果 相比于0 μmol/L SAMC组,25、50、100 μmol/L SAMC组HK-1和C666-1细胞PD-L1表达均显著下调(P<0.05),相比于0 μmol/L SAMC+CD8+T细胞组,25、50、100 μmol/L SAMC+CD8+T细胞组HK-1和C666-1细胞培养上清中INF-γ和TNF-α浓度均能显著增加,HK-1和C666-1细胞裂解率显著增加(P<0.01).相比于对照组,CD8+T细胞组和SAMC+CD8+T细胞组小鼠瘤体积和瘤重显著下降(P<0.05),小鼠血清INF-γ和TNF-α浓度显著增加,相比于CD8+T细胞组,SAMC+CD8+T细胞组小鼠瘤体积和瘤重显著下降(P<0.05),小鼠血清INF-γ和TNF-α浓度显著增加(P<0.05),肿瘤组织PD-L1表达显著下调(P<0.01).结论 SAMC可通过抑制人鼻咽癌细胞PD-L1表达而促进CD8+T细胞的杀伤功能.

OBJECTIVE To investigate the effect of SAMC on the killing function of CD8+T cells against nasopharyngeal carcinoma cells and its mechanism.METHODS HK-1 and C666-1 are divided into 0,25,50,and 100 mol/L SAMC group,Western blot was used to detcet PD-L1 expression in tumor cells.CD8+T cells were co-cultured with HK-1 and C666-1 cells in a ratio of 10∶1,and 0,25,50,and 100 μmol/L SAMC were added and detect the killing ability of CD8+T on HK-1 and C666-1.ELISA was used to detect INF-γ and TNF-α concentration.Construct a subcutaneous transplant tumor model of nasopharyngeal HK-1 cells,and divide it into a control group,CD8+T cell group,SAMC group,and SAMC+CD8+T cell group.The tumor volume was measured during treatment in each group of mice.Western blot was used to detect the expression of PD-L1 in the tumor tissue,ELISA was used to detect INF-γ and TNF-α concentration of mouse serum.RESULTS Compared to 0 μmol/L SAMC group,the expression of PD-L1 in 25,50,100μmol/L SAMC group were significantly downregulated(P<0.05).Compared to 0 μmol/L SAMC+CD8+T group,the INF-γ and TNF-α concentration were significantly increased in 25,50,100 μmol/L SAMC+CD8+T group,the lysis rates of HK-1 and C666-1 cells were significantly increased.Compared with the control group,the tumor volume and weight in the CD8+T cell group and SAMC+CD8+T cell group were significantly reduced(P<0.05),the concentration of INF-γ and TNF-α were significantly increased.Compared with the CD8+T cell group,the tumor volume and weight in the SAMC+CD8+T cell group mice significantly decreased(P<0.05),while the serum INF-γ and TNF-α concentration significantly increased(P<0.05),and the expression of PDL-1 in tumor tissue was significantly downregulated(P<0.01).CONCLUSION SAMC can promote the killing function of CD8+T cells by inhibiting the expression of PD-L1 in human nasopharyngeal carcinoma cells.

翟健;李军

唐山市人民医院头颈肿瘤外科,河北 唐山 063001

鼻咽癌酶联免疫吸附测定S-烯丙基巯基半胱氨酸细胞程序性死亡配体-1

Nasopharyngeal CarcinomaEnzyme-Linked Immunosorbent AssayS-Allylmercaptocysteineprogrammed cell death-ligand 1

《中国耳鼻咽喉头颈外科》 2024 (002)

74-78 / 5

河北省医学科学研究课题(20220572)

10.16066/j.1672-7002.2024.02.002

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