内质网应激对T细胞抗肿瘤功能调控的研究进展  

Research progress of T cell anti-tumor function regulated by endoplasmic reticulum stress

作　　者：王铮豪 高亚凤 张连军 刘畅[1] WANG Zhenghao;GAO Yafeng;ZHANG Lianjun;LIU Chang(School of Life Science and Technology,China Pharmaceutical University,Nanjing 211198;Suzhou Institute of Systems Medicine,Chinese Academy of Medical Sciences and Peking Union Medical College,Suzhou 215123,China)

机构地区：[1]中国药科大学生命科学与技术学院,南京211198 [2]中国医学科学院北京协和医学院苏州系统医学研究所,苏州215123

出　　处：《中国药科大学学报》2022年第5期518-524,共7页Journal of China Pharmaceutical University

基　　金：国家自然科学基金资助项目(No.81971466);江苏省杰出青年基金资助项目(No.BK20220049)。

摘　　要：内质网应激参与肿瘤的发生与发展,近年来,内质网应激对T细胞发育和功能调控的研究也逐渐深入。肿瘤微环境中浸润的T细胞内质网应激的发生加剧T细胞的耗竭,损害T细胞抗肿瘤免疫功能。内质网应激抑制剂的使用可以减轻T细胞的耗竭程度,改善肿瘤微环境中T细胞的抗肿瘤功能。此外,一些时钟基因如Per1和Per2的下调也促进了T细胞耗竭的进展,而内质网应激通路的效应分子能够调控生物钟网络中Per基因家族的转录,增强T细胞的免疫功能。本文就内质网应激调控T细胞的抗肿瘤功能进行论述,为肿瘤免疫治疗提供新策略。Endoplasmic reticulum(ER)stress is involved in the development and progression of tumors.In recent years,great attention has been paid to the study of the interplay of ER stress and T cell differentiation and functionality.Intense ER stress in the tumor-infiltrating T cells exacerbates T cell exhaustion and impairs T cell anti-tumor immunity.Therefore,a variety of ER stress inhibitors have been developed and utilized to alleviate T cell exhaustion,which improves T cell function in tumor microenvironment.Furthermore,the downregulation of several circadian clock genes like Per1 and Per2 also aggravates T cell exhaustion,and the key downstream effector molecules in ER stress regulate the transcription of Per family,thus enhancing the T cell function.In the present manuscript,we particularly summarize how ER stress impacts the anti-tumor immunity of T cells,and further discuss potential strategies for improving tumor immunotherapy via targeting ER stress.

关 键 词：内质网应激 T细胞 抗肿瘤功能 进展 

分 类 号：R392[医药卫生—免疫学] R73[医药卫生—基础医学]