摘要
T细胞耗竭是非小细胞肺癌(NSCLC)免疫治疗受限的主要原因,表现为效应功能丧失和抑制性受体高表达。其发生受TOX/TCF-1调控的转录与表观遗传重编程、多重抑制信号、代谢异常及免疫微环境共同影响。耗竭T细胞具有异质性,前体与终末亚群在功能和治疗响应中作用不同。联合阻断、代谢和表观遗传干预等策略有望逆转耗竭。
T cell exhaustion is a major factor limiting the efficacy of immunotherapy for NSCLC,characterized by loss of effector function and high expression of inhibitory receptors.Its development is influenced by transcriptional and epigenetic reprogramming regulated by TOX/TCF-1,multiple inhibitory signals,metabolic abnormalities,and the immune microenvironment.Exhausted T cells are heterogeneous,with precursor and terminal subsets playing different roles in function and therapeutic response.Strategies such as combined blockade,metabolic interventions,and epigenetic modulation hold promise to reverse exhaustion.
作者
白杰
马晓梅
阿木尔札亚
Bai Jie;Ma Xiaomei;Amuer Zhaya(Affiliated Tumor Hospital of Xinjiang Medical University,Urumqi,Xinjiang 830011,China)
出处
《首都食品与医药》
2026年第1期28-30,共3页
Capital Food Medicine
关键词
非小细胞肺癌
T细胞耗竭
免疫检查点抑制剂
Non-small cell lung cancer
T cell exhaustion
immune checkpoint inhibitors
