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

J Neuroimmunol. 2006 Nov;180(1-2):9-16. doi: 10.1016/j.jneuroim.2006.07.009. Epub 2006 Aug 14.


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

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis / immunology
  • Complement Membrane Attack Complex / immunology
  • Complement System Proteins / immunology*
  • Cytoprotection
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Encephalomyelitis, Autoimmune, Experimental / physiopathology
  • Humans
  • Inflammation / immunology*
  • Inflammation / physiopathology
  • Multiple Sclerosis / immunology*
  • Multiple Sclerosis / physiopathology
  • Nerve Fibers, Myelinated / immunology*
  • Nerve Fibers, Myelinated / metabolism
  • Nerve Fibers, Myelinated / pathology
  • Oligodendroglia / immunology


  • Complement Membrane Attack Complex
  • Complement System Proteins