Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, China; Department of Experimental Research, Sun Yat-sen University Cancer Center, State Key Laboratory Oncology in South China, Guangzhou, 510060, China.
Key Laboratory for Regenerative Medicine of Ministry of Education, Institute of Hematology, Jinan University, Guangzhou, 510632, China.
Eur J Pharmacol. 2020 Aug 15;881:173240. doi: 10.1016/j.ejphar.2020.173240. Epub 2020 Jun 1.
Study of the molecular mechanisms underlying cancer immune escape is one of the core issues in immuno-oncology research. Cancer cells can evade T cell cytotoxicity by exploiting the upregulation of T cell inhibitory receptors on T cells and their ligands on cancer cells. These upregulated proteins include the inhibitory receptor programmed cell-death protein 1 (PD-1) and its ligand programmed cell death 1 ligand 1 (PD-L1), which can induce T cell exhaustion and reduce T cell activation. Characterizing PD-1 regulation will help to elucidate the molecular mechanisms underlying T cell exhaustion and improve cancer treatment. Recent studies have found that tumor cells regulate PD-1 during gene transcription, post-transcriptional regulation, and post-translational modification and influence the effects of the anticancer immune response by targeting PD-1. In this review,we summarize the mechanisms of PD-1 regulation in T cells.
研究癌症免疫逃逸的分子机制是免疫肿瘤学研究的核心问题之一。癌细胞可以通过上调 T 细胞上的 T 细胞抑制受体及其在癌细胞上的配体来逃避 T 细胞的细胞毒性。这些上调的蛋白包括抑制受体程序性细胞死亡蛋白 1（PD-1）及其配体程序性细胞死亡配体 1（PD-L1），它们可诱导 T 细胞衰竭并降低 T 细胞激活。对 PD-1 调节的特征描述将有助于阐明 T 细胞衰竭的分子机制，并改善癌症治疗。最近的研究发现，肿瘤细胞在基因转录、转录后调控和翻译后修饰过程中调节 PD-1，并通过靶向 PD-1 影响抗肿瘤免疫反应的效果。在这篇综述中，我们总结了 T 细胞中 PD-1 调节的机制。
