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J Neuroimmunol. 2006 Nov;180(1-2):9-16. Epub 2006 Aug 14.

Complement activation in autoimmune demyelination: dual role in neuroinflammation and neuroprotection.

Author information

1
Department of Neurology, Baltimore MD, USA. hrus@umaryland.edu

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.

PMID:
16905199
DOI:
10.1016/j.jneuroim.2006.07.009
[Indexed for MEDLINE]

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