Role of Cytokines as Mediators and Regulators of Microglial Activity in Inflammatory Demyelination of the CNS

被引:72
作者
Merson, Tobias D. [1 ,2 ]
Binder, Michele D. [1 ,2 ]
Kilpatrick, Trevor J. [1 ,2 ]
机构
[1] Univ Melbourne, Florey Neurosci Inst, Parkville, Vic 3010, Australia
[2] Univ Melbourne, Ctr Neurosci, Parkville, Vic 3010, Australia
关键词
Microglia; Macrophages; Innate immunity; Cytokines; Interleukins; Interferons; Inflammatory demyelination; Multiple Sclerosis; Experimental autoimmune encephalomyelitis (EAE); Remyelination; Oligodendrocyte; Myelin; TUMOR-NECROSIS-FACTOR; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; GROWTH-FACTOR-BETA; COLONY-STIMULATING FACTOR; LEUKEMIA INHIBITORY FACTOR; NITRIC-OXIDE SYNTHASE; MULTIPLE-SCLEROSIS LESIONS; MESSENGER-RNA EXPRESSION;
D O I
10.1007/s12017-010-8112-z
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
As the resident innate immune cells of the central nervous system (CNS), microglia fulfil a critical role in maintaining tissue homeostasis and in directing and eliciting molecular responses to CNS damage. The human disease Multiple Sclerosis and animal models of inflammatory demyelination are characterized by a complex interplay between degenerative and regenerative processes, many of which are regulated and mediated by microglia. Cellular communication between microglia and other neural and immune cells is controlled to a large extent by the activity of cytokines. Here we review the role of cytokines as mediators and regulators of microglial activity in inflammatory demyelination, highlighting their importance in potentiating cell damage, promoting neuroprotection and enhancing cellular repair in a context-dependent manner.
引用
收藏
页码:99 / 132
页数:34
相关论文
共 455 条
[1]   Functional diversity of helper T lymphocytes [J].
Abbas, AK ;
Murphy, KM ;
Sher, A .
NATURE, 1996, 383 (6603) :787-793
[2]  
ADAMS DH, 1991, J IMMUNOL, V147, P609
[3]   The fibrin-derived γ377-395 peptide inhibits microglia activation and suppresses relapsing paralysis in central nervous system autoimmune disease [J].
Adams, Ryan A. ;
Bauer, Jan ;
Flick, Matthew J. ;
Sikorski, Shoana L. ;
Nuriel, Tal ;
Lassmann, Hans ;
Degen, Jay L. ;
Akassoglou, Katerina .
JOURNAL OF EXPERIMENTAL MEDICINE, 2007, 204 (03) :571-582
[4]   Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].
Aggarwal, S ;
Ghilardi, N ;
Xie, MH ;
de Sauvage, FJ ;
Gurney, AL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (03) :1910-1914
[5]   Oligodendrocyte apoptosis and primary demyelination induced by local TNF/p55TNF receptor signaling in the central nervous system of transgenic mice - Models for multiple sclerosis with primary oligodendrogliopathy [J].
Akassoglou, K ;
Bauer, J ;
Kassiotis, G ;
Pasparakis, M ;
Lassmann, H ;
Kollias, G ;
Probert, L .
AMERICAN JOURNAL OF PATHOLOGY, 1998, 153 (03) :801-813
[6]   Toll-like receptor signaling [J].
Akira, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (40) :38105-38108
[7]   Death ligands and autoimmune demyelination [J].
Aktas, Orhan ;
Prozorovski, Timour ;
Zipp, Frauke .
NEUROSCIENTIST, 2006, 12 (04) :305-316
[8]   Ciliary neurotrophic factor activates spinal cord astrocytes, stimulating their production and release of fibroblast growth factor-2, to increase motor neuron survival [J].
Albrecht, PJ ;
Dahl, JP ;
Stoltzfus, OK ;
Levenson, R ;
Levison, SW .
EXPERIMENTAL NEUROLOGY, 2002, 173 (01) :46-62
[9]   Interleukin-1 and neuronal injury [J].
Allan, SM ;
Tyrrell, PJ ;
Rothwell, NJ .
NATURE REVIEWS IMMUNOLOGY, 2005, 5 (08) :629-640
[10]  
Allione A, 1999, J IMMUNOL, V163, P4182