The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.
The programmed death-1 immune-suppressive pathway: barrier to antitumor immunity.
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DOI：
10.4049/jimmunol.1401572
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发表时间：
2014-10-15
期刊：
影响因子：
--
通讯作者：
Haile ST
中科院分区：
文献类型：
--
作者：
Ostrand-Rosenberg S;Horn LA;Haile ST
程序性死亡配体1（PD - L1，也称为B7同源体1（B7 - H1）或CD274）是抗肿瘤免疫的一个主要障碍，因为它：（i）通过与其受体PD - 1（CD279）结合，使肿瘤反应性T细胞产生耐受/失能；（ii）使肿瘤细胞对CD8 + T细胞和FasL介导的裂解产生抗性；（iii）通过T细胞表达的CD80的反向信号传导使T细胞产生耐受。PD - L1大量存在于肿瘤微环境中，许多恶性细胞以及免疫细胞和血管内皮细胞都表达它。PD - L1在阻碍抗肿瘤免疫中的关键作用已在多个动物模型以及近期的临床试验中得到证实。本文综述了PD - L1损害抗肿瘤免疫的机制，并讨论了在肿瘤微环境中存在表达PD - L1的细胞的情况下维持T细胞活化的已确立的和实验性的策略。
Programmed Death Ligand 1 (PD-L1, also known as B7 homolog 1 (B7-H1) or CD274) is a major obstacle to anti-tumor immunity because it (i) tolerizes/anergizes tumor-reactive T cells by binding to its receptor PD-1 (CD279); (ii) renders tumor cells resistant to CD8+ T cell and FasL-mediated lysis; and (iii) tolerizes T cells by reverse signalling through T cell-expressed CD80. PD-L1 is abundantly present in the tumor microenvironment where it is expressed by many malignant cells as well as by immune cells and vascular endothelial cells. The critical role of PD-L1 in obstructing anti-tumor immunity has been demonstrated in multiple animal models and in recent clinical trials. This article reviews the mechanisms by which PD-L1 impairs anti-tumor immunity and discusses established and experimental strategies for maintaining T cell activation in the presence of PD-L1-expressing cells in the tumor microenvironment.
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影响因子：
17.1
作者：
Amarnath S;Mangus CW;Wang JC;Wei F;He A;Kapoor V;Foley JE;Massey PR;Felizardo TC;Riley JL;Levine BL;June CH;Medin JA;Fowler DH
通讯作者：
Fowler DH
影响因子：
11.2
作者：
Blank, C;Brown, I;Gajewski, TF
通讯作者：
Gajewski, TF
影响因子：
10.1
作者：
Haile ST;Horn LA;Ostrand-Rosenberg S
通讯作者：
Ostrand-Rosenberg S
PD-L1 的过度表达与人类肝细胞癌的肿瘤侵袭性和术后复发显着相关。
影响因子：
11.5
作者：
Gao, Qiang;Wang, Xiao-Ying;Fan, Jia
通讯作者：
Fan, Jia
DOI：
10.1084/jem.20090847
发表时间：
2009-12-21
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Francisco LM;Salinas VH;Brown KE;Vanguri VK;Freeman GJ;Kuchroo VK;Sharpe AH
通讯作者：
Sharpe AH