Polarization of macrophages and microglia in inflammatory demyelination

被引:75
作者
Cao, Li [1 ]
He, Cheng
机构
[1] Second Mil Med Univ, Changzheng Hosp, Inst Neurosci, Shanghai 200433, Peoples R China
基金
中国国家自然科学基金;
关键词
macrophage; microglia; polarization; demyelination; remyelination; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MULTIPLE-SCLEROSIS LESIONS; TUMOR-NECROSIS-FACTOR; MYELIN PHAGOCYTOSIS; ALTERNATIVE ACTIVATION; SODIUM-CHANNELS; NITRIC-OXIDE; LEWIS RATS; IN-VITRO; T-CELLS;
D O I
10.1007/s12264-013-1324-0
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system, and microglia and macrophages play important roles in its pathogenesis. The activation of microglia and macrophages accompanies disease development, whereas depletion of these cells significantly decreases disease severity. Microglia and macrophages usually have diverse and plastic phenotypes. Both pro-inflammatory and antiinflammatory microglia and macrophages exist in MS and its animal model, experimental autoimmune encephalomyelitis. The polarization of microglia and macrophages may underlie the differing functional properties that have been reported. in this review, we discuss the responses and polarization of microglia and macrophages in MS, and their effects on its pathogenesis and repair. Harnessing their beneficial effects by modulating their polarization states holds great promise for the treatment of inflammatory demyelinating diseases.
引用
收藏
页码:189 / 198
页数:10
相关论文
共 89 条
[1]   Immunohistochemical study of arginase-1 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis [J].
Ahn, Meejung ;
Yang, Wonjun ;
Kim, Heechul ;
Jin, Jae-Kwang ;
Moon, Changjong ;
Shin, Taekyun .
BRAIN RESEARCH, 2012, 1453 :77-86
[2]   Relapsing and remitting multiple sclerosis: Pathology of the newly forming lesion [J].
Barnett, MH ;
Prineas, JW .
ANNALS OF NEUROLOGY, 2004, 55 (04) :458-468
[3]   PHAGOCYTIC-ACTIVITY OF MACROPHAGES AND MICROGLIAL CELLS DURING THE COURSE OF ACUTE AND CHRONIC RELAPSING EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS [J].
BAUER, J ;
SMINIA, T ;
WOUTERLOOD, FG ;
DIJKSTRA, CD .
JOURNAL OF NEUROSCIENCE RESEARCH, 1994, 38 (04) :365-375
[4]   Antigen presentation in autoimmunity and CNS inflammation: how T lymphocytes recognize the brain [J].
Becher, Burkhard ;
Bechmann, Ingo ;
Greter, Melanie .
JOURNAL OF MOLECULAR MEDICINE-JMM, 2006, 84 (07) :532-543
[5]   Axonal protection using flecainide in experimental autoimmune encephalomyelitis [J].
Bechtold, DA ;
Kapoor, R ;
Smith, KJ .
ANNALS OF NEUROLOGY, 2004, 55 (05) :607-616
[6]   Sodium channels and microglial function [J].
Black, Joel A. ;
Waxman, Stephen G. .
EXPERIMENTAL NEUROLOGY, 2012, 234 (02) :302-315
[7]   Sodium Channel Activity Modulates Multiple Functions in Microglia [J].
Black, Joel A. ;
Liu, Shujun ;
Waxman, Stephen G. .
GLIA, 2009, 57 (10) :1072-1081
[8]   Microglia-mediated neurotoxicity: uncovering the molecular mechanisms [J].
Block, Michelle L. ;
Zecca, Luigi ;
Hong, Jau-Shyong .
NATURE REVIEWS NEUROSCIENCE, 2007, 8 (01) :57-69
[9]   Myelin-laden macrophages are anti-inflammatory, consistent with foam cells in multiple sclerosis [J].
Boven, LA ;
Van Meurs, M ;
Van Zwam, M ;
Wierenga-Wolf, A ;
Hintzen, RQ ;
Boot, RG ;
Aerts, JM ;
Amor, S ;
Nieuwenhuis, EE ;
Laman, JD .
BRAIN, 2006, 129 :517-526
[10]   Induction and blockage of oligodendrogenesis by differently activated microglia in an animal model of multiple sclerosis [J].
Butovsky, O ;
Landa, G ;
Kunis, G ;
Ziv, Y ;
Avidan, H ;
Greenberg, N ;
Schwartz, A ;
Smirnov, I ;
Pollack, A ;
Jung, S ;
Schwartz, M .
JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (04) :905-915