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The role of CD47-SIRPα immune checkpoint in tumor immune evasion and innate immunotherapy
Life Sciences ( IF 5.2 ) Pub Date : 2021-03-01 , DOI: 10.1016/j.lfs.2021.119150
Zihao Li , Yue Li , Jing Gao , Yilin Fu , Peiyan Hua , Yingying Jing , Mingjun Cai , Hongda Wang , Ti Tong

As a transmembrane protein, CD47 plays an important role in mediating cell proliferation, migration, phagocytosis, apoptosis, immune homeostasis, inhibition of NO signal transduction and other related reactions. Upon the interaction of innate immune checkpoint CD47-SIRPα occurrence, they send a “don't eat me” signal to the macrophages. This signal ultimately helps tumors achieve immune escape by inhibiting macrophage contraction to prevent tumor cells from phagocytosis. Therefore, the importance of CD47-SIRPα immune checkpoint inhibitors in tumor immunotherapy has attracted more attention in recent years. Based on the cognitive improvement of the effect with CD47 in tumor microenvironment and tumor characteristics, the pace of tumor treatment strategies for CD47-SIRPα immune checkpoint inhibitors has gradually accelerated. In this review, we introduced the high expression of CD47 in cancer cells to avoid phagocytosis by immune cells and the importance of CD47 in the structure of cancer microenvironment and the maintenance of cancer cell characteristics. Given the role of the innate immune system in tumorigenesis and development, an improved understanding of the anti-tumor process of innate immune checkpoint inhibitors can lay the foundation for more effective combinations with other anti-tumor treatment strategies.



中文翻译:

CD47-SIRPα免疫检查点在肿瘤免疫逃逸和先天免疫治疗中的作用

CD47作为跨膜蛋白,在介导细胞增殖,迁移,吞噬作用,细胞凋亡,免疫稳态,抑制NO信号转导及其他相关反应中起重要作用。在先天免疫检查点CD47-SIRPα相互作用后,它们向巨噬细胞发出“不要吃我”的信号。该信号最终通过抑制巨噬细胞收缩来防止肿瘤细胞吞噬,从而帮助肿瘤实现免疫逃逸。因此,近年来CD47-SIRPα免疫检查点抑制剂在肿瘤免疫治疗中的重要性引起了越来越多的关注。基于CD47在肿瘤微环境中的作用和肿瘤特征的认知改善,CD47-SIRPα免疫检查点抑制剂的肿瘤治疗策略已逐渐加快。在这篇评论中,我们介绍了CD47在癌细胞中的高表达以避免免疫细胞的吞噬作用,以及CD47在癌症微环境的结构和维持癌细胞特征中的重要性。鉴于先天免疫系统在肿瘤发生和发展中的作用,对先天免疫检查点抑制剂的抗肿瘤过程的更好理解可以为与其他抗肿瘤治疗策略更有效组合奠定基础。

更新日期:2021-03-04
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