CD226、 TIGIT和CD96调节NK细胞功能参与机体抗肿瘤免疫  

CD226,TIGIT and CD96 regulate NK cell function and participate in anti-tumor immunity

作　　者：张慧媛 刘睿言 张宇丝 刘晓斌[1] 陈丽华 ZHANG Huiyuan;LIU Ruiyan;ZHANG Yusi;LIU Xiaobin;CHEN Lihua(Medical School of Yan'an University,Yan'an 716000;Department of Immunology,Basic Medical Science Academy,Air Force Medical University,Xi'an 710032,China;Cadet Regiment,Basic Medical Science Academy,Air Force Medical University,Xi'an 710032,China)

机构地区：[1]延安大学医学院,陕西延安716000 [2]空军军医大学基础医学院免疫学教研室,陕西西安710032 [3]空军军医大学基础医学院学员旅,陕西西安710032

出　　处：《细胞与分子免疫学杂志》2023年第9期852-856,共5页Chinese Journal of Cellular and Molecular Immunology

基　　金：国家自然科学基金(82071848);国家自然科学基金青年项目(81901600)。

摘　　要：CD226是自然杀伤(NK)细胞表面的活化性受体,与具有免疫球蛋白和免疫受体酪氨酸抑制基序结构域的T细胞免疫受体(TIGIT)和CD96等分子通过竞争结合肿瘤细胞表面的CD155等配体,介导NK细胞的杀伤功能。虽然TIGIT和CD96在肿瘤微环境中有其他结合配体,但它们以更高的亲和力竞争结合CD115配体,并抑制NK细胞的活性,使肿瘤细胞逃避杀伤。因此,研究这三种NK细胞表面受体在不同肿瘤中的表达模式,并监测分析它们与配体的结合能力,有助于探索新的肿瘤治疗策略。本文总结了CD226、 TIGIT和CD96等NK细胞受体分子调节NK细胞功能在机体抗肿瘤免疫应答中的作用及其机制。CD226 is an activated receptor on the surface of natural killer(NK)cells.It competes with TIGIT and CD96 to bind to ligands such as CD155 on the surface of tumor cells and mediates the killing function of NK cells.Although TIGIT and CD96 have other binding ligands in the tumor microenvironment,they compete to bind CD115 ligands with higher affinity and inhibit the activity of NK cells,which allows tumor cells to evade killing.Therefore,studying the expression patterns of these three NK cell surface receptors in different tumors and monitoring their binding ability with ligands will help us to explore new tumor treatment strategies.This article reviews the role and mechanism of CD226,TIGIT,CD96 and other NK cell receptor molecules in regulating NK cell function in anti-tumor immune response.

关 键 词：肿瘤免疫应答 自然杀伤(NK)细胞 CD226 TIGIT CD96 综述 

分 类 号：S853.53[农业科学—临床兽医学] R392[农业科学—兽医学] R392.11[农业科学—畜牧兽医] G353.11[医药卫生—免疫学]