CD8+T细胞在肝细胞癌中的耗竭机制
The mechanism of CD8+T cell exhaustion in hepatocellular carcinoma
荆郭 1詹天诚 1宋万骞 1袁永康 1康宁 1张强1
作者信息
摘要
在肝细胞癌(hepatocellular carcinoma,HCC)中,抗原的持续刺激会使CD8+T细胞呈现耗竭状态,具体表现为CD8+T细胞表面抑制性受体(inhibitory receptors,IRs)持续性表达上调及共表达、表观遗传和转录谱发生改变,以及代谢呈现紊乱状态等,导致CD8+T细胞的增殖功能衰退,免疫功能逐渐丧失,进而引起CD8+T细胞死亡,最终使肿瘤细胞发生免疫逃逸.本文综述了目前对CD8+T细胞耗竭特征及机制的最新研究进展,为靶向耗竭CD8+T细胞的HCC免疫治疗提供借鉴.
Abstract
Under continuous antigen stimulation in hepatocellular carcinoma,CD8+T cells undergo an exhausted state through various mechanisms,which is characterized by sustained upregulation and co-expression of inhibitory receptors on the surface of CD8+T cells,as well as changes in epigenetic and transcriptional profiles,and metabolic disorders.These factors cause impaired proliferation function of CD8+T cells,progressive loss of immune function,and ultimately CD8+T cell death,resulting in immune escape of tumor cells.This article provides a review of the latest research progress on the occurrence,development,characteristics,and potential mechanisms of CD8+T cell exhaustion in hepatocellular carcinoma.It aims to serve as a reference for further mechanism research and targeted treatment of CD8+T cell exhaustion in hepatocellular carcinoma.
关键词
CD8+T细胞耗竭/肝细胞癌/抑制性受体/肿瘤微环境Key words
CD8+T cell exhaustion/hepatocellular carcinoma/inhibitory receptor/tumor microenvironment引用本文复制引用
基金项目
国家自然科学基金项目(82104461)
国家自然科学基金项目(8227-4221)
国家级大学生创新创业训练计划项目(20231-0063010)
出版年
2024
NETL
NSTL
万方数据