Abstract
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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis / immunology
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Complement Membrane Attack Complex / immunology
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Complement System Proteins / immunology*
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Cytoprotection
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Encephalomyelitis, Autoimmune, Experimental / immunology*
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Encephalomyelitis, Autoimmune, Experimental / physiopathology
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Humans
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Inflammation / immunology*
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Inflammation / physiopathology
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Multiple Sclerosis / immunology*
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Multiple Sclerosis / physiopathology
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Nerve Fibers, Myelinated / immunology*
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Nerve Fibers, Myelinated / metabolism
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Nerve Fibers, Myelinated / pathology
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Oligodendroglia / immunology
Substances
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Complement Membrane Attack Complex
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Complement System Proteins