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趋化因子受体CCR7依赖的树突状细胞迁移的调控机制 被引量:10

Molecular regulation of CCR7-mediated dendritic cell migration
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摘要 树突状细胞(DC)是机体功能最为强大的抗原提呈细胞,不仅能够活化获得性免疫以促进机体对病原的清除,还能够诱导免疫耐受,维持免疫稳态。树突状细胞在不同免疫器官的定位及迁移是其发挥免疫功能和维持机体稳态的基础。外周的未成熟DC摄取病原体后成熟活化,上调趋化因子受体CCR7的表达。由淋巴结基质细胞所分泌的趋化因子CCL19/CCL21作用于DC表达的CCR7,促进DC向次级淋巴器官的T细胞区迁移,启动并调控T细胞介导的获得性免疫应答。CCR7信号触发一系列胞内信号通路,并受到胞内骨架系统、代谢通路及表观修饰等多种层面的调控。越来越多的研究表明DC迁移的紊乱可能导致DC在炎症部位的过度聚集及活化,引起组织过度炎症,甚至引发自身免疫性疾病。在这篇综述中,我们将讨论DC迁移过程的调控机制及其在炎症性疾病、自身免疫性疾病等免疫相关疾病中作用的研究进展。 As the most powerful antigen-presenting cells,dendritic cells(DCs)not only activate acquired immunity for the clearance of pathogens,but also induce immune tolerance and maintain immune homeostasis.The localization and migration of DC between different organs is critical for immune function and homeostasis.Immature DC undergoes maturation and upregulates the expression of chemokine receptor CCR7 upon sensing of pathogenic or injury signals through pattern-recognition receptor.Chemokine CCL19/CCL21 secreted by lymph node stromal cells acts on CCR7,and promotes the migration of DC toward secondary lymphatic organs to initiate T cell-mediated acquired immune response.CCR7 stimulation triggers a series of intracellular signaling pathway,which are regulated by multiple mechanisms,such as intracellular skeletal systems,metabolic pathways,and epigenetic modifications.Increasing studies show that the disorders of DC migration may lead to excessive aggregation and activation of DCs in the inflammatory tissues,causing excessive inflammation and even autoimmune diseases.In this review,we will discuss the regulatory mechanism of DC migration and its role in immune related diseases such as inflammatory diseases and autoimmune diseases.
作者 程玉洁 刘娟(指导) CHENG Yu-Jie;LIU Juan(National Key Laboratory of Medical Immunology and Institute of Immunology,Navy Medical University,Shanghai 200433,China)
出处 《中国免疫学杂志》 CAS CSCD 北大核心 2020年第8期1004-1008,共5页 Chinese Journal of Immunology
基金 国家自然科学基金优秀青年科学基金项目(31622024)资助。
关键词 树突状细胞 趋化因子受体CCR7 自身免疫性疾病 免疫调控 Dendritic cells Chemokine receptor CCR7 Autoimmune diseases Immune regulation
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