Role of the tumor microenvironment in PD-L1/PD-1-mediated tumor immune escape

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作者
Xianjie Jiang
Jie Wang
Xiangying Deng
Fang Xiong
Junshang Ge
Bo Xiang
Xu Wu
Jian Ma
Ming Zhou
Xiaoling Li
Yong Li
Guiyuan Li
Wei Xiong
Can Guo
Zhaoyang Zeng
机构
[1] Central South University,NHC Key Laboratory of Carcinogenesis (Central South University) and Hunan Key Laboratory of Translational Radiation Oncology, Hunan Cancer Hospital and the Affiliated Cancer Hospital of Xiangya School of Medicine
[2] Central South University,The Key Laboratory of Carcinogenesis and Cancer Invasion of the Chinese Ministry of Education, Cancer Research Institute and School of Basic Medical Science
[3] The Third Xiangya Hospital,Hunan Key Laboratory of Nonresolving Inflammation and Cancer, Disease Genome Research Center
[4] Central South University,Department of Chemistry
[5] University of North Dakota,Department of Cancer Biology
[6] Lerner Research Institute,undefined
[7] Cleveland Clinic,undefined
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关键词
Tumor immune escape; PD-L1; PD-1; Tumor microenvironment; Inflammatory factor;
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摘要
Tumor immune escape is an important strategy of tumor survival. There are many mechanisms of tumor immune escape, including immunosuppression, which has become a research hotspot in recent years. The programmed death ligand-1/programmed death-1 (PD-L1/PD-1) signaling pathway is an important component of tumor immunosuppression, which can inhibit the activation of T lymphocytes and enhance the immune tolerance of tumor cells, thereby achieving tumor immune escape. Therefore, targeting the PD-L1/PD-1 pathway is an attractive strategy for cancer treatment; however, the therapeutic effectiveness of PD-L1/PD-1 remains poor. This situation requires gaining a deeper understanding of the complex and varied molecular mechanisms and factors driving the expression and activation of the PD-L1/PD-1 signaling pathway. In this review, we summarize the regulation mechanisms of the PD-L1/PD-1 signaling pathway in the tumor microenvironment and their roles in mediating tumor escape. Overall, the evidence accumulated to date suggests that induction of PD-L1 by inflammatory factors in the tumor microenvironment may be one of the most important factors affecting the therapeutic efficiency of PD-L1/PD-1 blocking.
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