CNS Remyelination and the Innate Immune System

被引:47
作者
McMurran, Christopher E. [1 ]
Jones, Clare A. [2 ]
Fitzgerald, Denise C. [3 ]
Franklin, Robin J. M. [1 ]
机构
[1] Univ Cambridge, Wellcome Trust Med Res Council, Cambridge Stem Cell Inst, Cambridge, England
[2] MedImmune, Cambridge, England
[3] Queens Univ Belfast, Sch Med Dent & Biomed Sci, Ctr Infect & Immun, Belfast, Antrim, North Ireland
基金
英国生物技术与生命科学研究理事会; 英国惠康基金;
关键词
remyelination; inflammation; innate immune system; microglia; macrophage; CUPRIZONE-INDUCED DEMYELINATION; MULTIPLE-SCLEROSIS; AUTOIMMUNE ENCEPHALOMYELITIS; PROGENITOR CELLS; MYELIN DEBRIS; MICROGLIA; ACTIVATION; MONOCYTES; MODEL; RAT;
D O I
10.3389/fcell.2016.00038
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
A misguided inflammatory response is frequently implicated in myelin damage. Particularly prominent among myelin diseases, multiple sclerosis (MS) is an autoimmune condition, with immune-mediated damage central to its etiology. Nevertheless, a robust inflammatory response is also essential for the efficient regeneration of myelin sheaths after such injury. Here, we discuss the functions of inflammation that promote remyelination, and how these have been experimentally disentangled from the pathological facets of the immune response. We focus on the contributions that resident microglia and monocyte-derived macrophages make to remyelination and compare the roles of these two populations of innate immune cells. Finally, the current literature is framed in the context of developing therapies that manipulate the innate immune response to promote remyelination in clinical myelin disease.
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页数:8
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