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中枢神经系统中被替代激活的小胶质细胞和巨噬细胞。

Alternatively activated microglia and macrophages in the central nervous system.

机构信息

Molecular Neurobiology Laboratory, Department of Biochemistry and Molecular Biology, Faculty of Biology, University of Barcelona, Barcelona, Spain; Centro Investigación Biomédica en Red: Enfermedades Neurodegenerativas (CIBERNED), Spain.

Division of Molecular Neurobiology, Department of Neuroscience, Karolinska Institute, 17177 Stockholm, Sweden.

出版信息

Prog Neurobiol. 2015 Aug;131:65-86. doi: 10.1016/j.pneurobio.2015.05.003. Epub 2015 Jun 8.

DOI:10.1016/j.pneurobio.2015.05.003
PMID:26067058
Abstract

Macrophages are important players in the fight against viral, bacterial, fungal and parasitic infections. From a resting state they may undertake two activation pathways, the classical known as M1, or the alternative known as M2. M1 markers are mostly mediators of pro-inflammatory responses whereas M2 markers emerge for resolution and cleanup. Microglia exerts in the central nervous system (CNS) a function similar to that of macrophages in the periphery. Microglia activation and proliferation occurs in almost any single pathology affecting the CNS. Often microglia activation has been considered detrimental and drugs able to stop microglia activation were considered for the treatment of a variety of diseases. Cumulative evidence shows that microglia may undergo the alternative activation pathway, express M2-type markers and contribute to neuroprotection. This review focuses on details about the role of M2 microglia and in the approaches available for its identification. Approaches to drive the M2 phenotype and data on its potential in CNS diseases are also reviewed.

摘要

巨噬细胞是对抗病毒、细菌、真菌和寄生虫感染的重要参与者。从静止状态来看,它们可能会经历两种激活途径,即经典的 M1 途径,或称为 M2 的替代途径。M1 标志物主要是促炎反应的介质,而 M2 标志物则出现以解决和清理问题。小胶质细胞在中枢神经系统 (CNS) 中发挥类似于外周巨噬细胞的功能。几乎任何一种影响中枢神经系统的单一病理学都会导致小胶质细胞的激活和增殖。通常情况下,小胶质细胞的激活被认为是有害的,能够阻止小胶质细胞激活的药物被认为可用于治疗各种疾病。越来越多的证据表明,小胶质细胞可能会经历替代激活途径,表达 M2 型标志物,并有助于神经保护。本综述重点介绍了 M2 小胶质细胞的作用细节及其鉴定方法。还综述了驱动 M2 表型的方法以及其在中枢神经系统疾病中的潜在作用的数据。

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