Regulation of PD-1 in T cells for cancer immunotherapy

被引:35
作者
Yu, Xibao [1 ,2 ]
Gao, Rili [1 ]
Li, Yangqiu [1 ]
Zeng, Chengwu [1 ]
机构
[1] Jinan Univ, Inst Hematol, Key Lab Regenerat Med, Minist Educ, Guangzhou 510632, Peoples R China
[2] Sun Yat Sen Univ, Dept Expt Res, State Key Lab Oncol South China, Canc Ctr, Guangzhou 510060, Peoples R China
基金
中国国家自然科学基金;
关键词
T cell exhaustion; Immunotherapy; PD-1; PD-L1; INHIBITORY RECEPTOR PD-1; CHRONIC HEPATITIS-B; DILATED CARDIOMYOPATHY; PROGRAMMED DEATH-1; VIRUS-INFECTION; TUMOR-CELLS; EXPRESSION; SUPPRESSOR; SURFACE; EFFICACY;
D O I
10.1016/j.ejphar.2020.173240
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Study of the molecular mechanisms underlying cancer immune escape is one of the core issues in immunooncology 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.
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页数:7
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