CCL20在脑卒中的发病机制及临床意义  

The Pathogenesis and Clinical Significance of CCL20 in Cerebral Stroke

作　　者：吕会娟[1] 孙伟[1] 孟德龙[1] 辛亭[1] 苏志强[1] 

机构地区：[1]哈尔滨医科大学附属第一医院神经内科,黑龙江哈尔滨150001

出　　处：《现代生物医学进展》2015年第13期2585-2587,共3页Progress in Modern Biomedicine

摘　　要：CCL20(C-C chemokine ligand 20)是CC亚族的趋化因子,曾被称为巨噬细胞炎症蛋白3α(MIP-3α)、肝脏活化调节趋化因子(LARC)和Exodus-1,与其唯一受体CC趋化因子受体6(CC chemokine receptor 6,CCR6)特异性结合,调节细胞的激活、趋化和迁移,参与形态发生、组织稳态、固有和获得性免疫以及许多疾病的炎症病理过程。在中枢神经中,CCL20与CCR6结合后激活小胶质细胞,其可应激相关性蛋白,形成持续性神经毒性级联反应,从而进一步损害周围神经元和脑组织,进而引起一系列的神经功能损伤症状。目前有关CCL20在脑卒中的日益引起人们的关注,深入研究其在脑卒中的作用,有可能为进一步揭示脑卒中的发病机制并为寻求有效的防治措施提供重要的理论基础。本文概述了CCL20的作用,重点阐述了其在脑卒中的作用。CCL20 （C-C chemokine ligand 20）, a chemokine of CC chemokines, also known as liver and activation-regulated chemokine （LARC）, macrophage inflammatory protein-3a （MIP-3a） or Exodus-l, is the only chemokine known to interact with CC chemokine receptor 6 （CCR6）, regulates cells activation, and migration, is involved in morphogenesis, homeostasis, innate and adaptive immunity and the inflammation pathological process in numerous of diseases. In the centre nervous system, CCL20, combined with CCR6, activates microglia and the cells produces other stress-related proteins, and evokes the self-perpetuating neurotoxicity cascade, which may damage surrounding neurons and brain tissues. Now the effect of CCL20 in the stroke are increasingly receiving attention. Thoroughly studying the effect of CCL20 in the stroke may further reveal the pathogenesis of stroke and provide important theoretical foundation for seeking effective prevention and treatment measures. It takes part in inflammatory response in the stroke. This article summarizes the effect of CCL20, and focuses on the roles of CCL20 in the stroke.

关 键 词：CCL20 脑缺血 脑出血 蛛网膜下腔出血 

分 类 号：R743.3[医药卫生—神经病学与精神病学]