Complement activation in autoimmune demyelination: dual role in neuroinflammation and neuroprotection.
Multiple sclerosis and its animal model experimental allergic encephalomyelitis are inflammatory demyelinating diseases of the central nervous system mediated by activated lymphocytes, macrophages/microglia and the complement system. Complement activation and the C5b-9 terminal complex contribute to the pathogenesis of these diseases through its role to promote demyelination. C5b-9 was also shown to protect oligodendrocytes from apoptosis both in vitro and in vivo. Our findings indicate that activation of complement and C5b-9 assembly plays a pro-inflammatory role in the acute phase, but may also be neuroprotective.
Rus
Horea
H
Department of Neurology, Baltimore MD, USA. hrus@umaryland.edu
Cudrici
Cornelia
C
Niculescu
Florin
F
Shin
Moon L
ML
D000818:Animals; D017209:Apoptosis / Q000276:immunology; D015938:Complement Membrane Attack Complex / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology*; D019610:Cytoprotection; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000503:physiopathology; D009103:Multiple Sclerosis / Q000276:immunology* / Q000503:physiopathology; D009413:Nerve Fibers, Myelinated / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D009836:Oligodendroglia / Q000276:immunology
D015938:Complement Membrane Attack Complex; D003165:Complement System Proteins