Abstract
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.
Highlights
Tumor immune escape refers to the phenomenon by which tumor cells can grow and metastasize by avoiding recognition and attack by the immune system through various mechanisms, which is an important strategy for tumor survival and development [1].The are many inducible factors of tumor immune escape, including the low immunogenicity of tumor cells, recognition of tumorspecific antibodies as autoantigens, tumor surface antigen modulation, tumor-induced exemption regions, and tumor-induced immunosuppression, the latter of which has been the most extensively studied mechanism to date
In T-ALL cells, we found that MYC can be directly combined with the PD-L1 promoter to upregulate the expression of PD-L1 [104], suggesting that the Epithelial growth factor receptor (EGFR) pathway could up-regulate the expression of the MYC transcription factor and promote its nuclear translocation to up-regulate the expression of PD-L1
Immune escape mediated by the PD-L1/Programmed death-1 (PD-1) signaling pathway has emerged as a hot topic in anti-tumor research and in the field of cancer translational medicine
Summary
Tumor immune escape refers to the phenomenon by which tumor cells can grow and metastasize by avoiding recognition and attack by the immune system through various mechanisms, which is an important strategy for tumor survival and development [1].The are many inducible factors of tumor immune escape, including the low immunogenicity of tumor cells, recognition of tumorspecific antibodies as autoantigens, tumor surface antigen modulation, tumor-induced exemption regions, and tumor-induced immunosuppression, the latter of which has been the most extensively studied mechanism to date. Recent studies have shown that many cytokines and tumor-derived exosomes in the tumor microenvironment can induce the expression of PD-L1 and promote tumor immune escape. Tregs and Bregs are immunosuppressive cells in the immune system that secrete IL-10, IL-35, and transforming growth factor (TGF)-β to IL-19, thereby playing an important role in promoting tumor cell proliferation and migration [40, 41].
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