CD8＋T细胞耗竭的细胞及分子机制研究进展

Cellular and molecular mechanism of CD8＋ T cell exhaustion

在慢性炎性反应及肿瘤进展过程中，T细胞持续暴露于炎性因子及抗原中，导致T细胞功能退化，即T细胞耗竭。功能耗竭的T细胞其效应功能受损，表达大量抑制性受体，且转录调控机制也发生显著改变。T细胞耗竭会影响机体对持续感染及肿瘤的有效控制，而逆转耗竭T细胞的功能有助于恢复机体正常的免疫效应。现以CD8＋ T细胞为代表，总结CD8＋ T细胞耗竭相关细胞及分子机制研究进展，以及相关抗感染及肿瘤的新的治疗策略。

T-cell exhaustion is characterized by the stepwise and progressive loss of T cell functions under conditions of antigen-persistence, which occurs following chronic infections and tumor outgrowth. Exhausted T cells present functional defects, express muhiple inhibitory receptors and show reprogrammed transcriptional regulation. As T cell exhaustion is correlated to its dysfunction to control infections and tumors, exploring new strategies to target exhausted T cell may reverse this dysfunctional state and reinvigorate immune response. This study takes CDs~ T cell as an example, which acts as an important subset involved in exhaustion state, discuss current understanding of the properties of exhausted T cell and the mechanisms that promote and maintain this state, and reveal new therapeutic targets for chronic infection and cancer.