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作 者:晏黎 黄伟[1] 全紫瑶 崔天盆[1] YAN Li;HUANG Wei;QUAN Zi-Yao;CUI Tian-Pen(Department of Laboratory Medicine,Wuhan Traditional Chinese and Western Medicine Hospital,Hubei University of Chinese Medicine,Wuhan 430022,China)
机构地区:[1]湖北中医药大学附属武汉市中西医结合医院检验科,武汉430022 [2]湖北中医药大学检验学院,武汉430065
出 处:《中国免疫学杂志》2021年第12期1517-1520,共4页Chinese Journal of Immunology
基 金:国家自然科学基金项目(81770038,81903217);湖北省卫生健康科研基金资助(WJ2019Z001);武汉市临床医学科研项目重点项目(WX17-A01)。
摘 要:机体在病毒感染、肿瘤等病理因素下产生的大量坏死细胞需要细胞毒性T淋巴细胞(CTL)的靶向杀伤作用来清除。人外周血BDCA3+树突状细胞上的Clec9A能特异性识别与结合坏死细胞暴露的纤维状肌动蛋白(F-actin),激活胞内脾酪氨酸激酶Syk。Clec9A作为F-actin的受体,不仅内吞坏死细胞,同时将坏死细胞相关抗原交叉提呈至CD8^(+)T细胞,活化CTL,启动机体获得性免疫应答。CTL释放的穿孔素及颗粒酶特异性杀伤靶细胞,导致体内感染细胞或肿瘤细胞进一步被清除。因此,Clec9A在机体抗病毒感染、肿瘤治疗中具有潜在的应用前景。A large number of necrotic cells produced by the pathological factors such as virus infection and tumor,which need to be clearanced by the targeted killing effect of cytotoxic T lymphocytes(CTL). C-type lectin domain family 9 A(Clec9 A,or DNGR-1)on human blood BDCA3+dendritic cells can specifically identify and bind F-actin exposed by necrotic cells,activate the spleen tyrosine-based kinase(Syk)pathway. As the receptor of F-actin,Clec9 A not only phagocytosis necrotic cells,but also cross-presents necrosis-related antigens to CD8^(+)T cells,which results in the activation CTL and initiates the adaptive immune response. Perforin and granzyme released by CTL further damage infected tissue cells or tumor cells,leading to apoptosis and necrosis of the injured cells and further clearance. Therefore,Clec9 A has a potential application prospect in anti-viral,tumor therapy.
关 键 词:C型凝集素9家族A成员 纤维状肌动蛋白 坏死细胞 交叉提呈
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