Cutting edge: C3, a key component of complement activation, is not required for the development of myelin oligodendrocyte glycoprotein peptide-induced experimental autoimmune encephalomyelitis in mice. Academic Article uri icon

Overview

abstract

  • Experimental autoimmune encephalomyelitis (EAE), an inflammatory demyelinating disease of the CNS, is regarded as an experimental model for multiple sclerosis. The complement has been implicated in the pathogenesis of multiple sclerosis. To clarify the role of C in mouse EAE, we immunized mice deficient in C3 (C3(-/-)) and their wild-type (C3(+/+)) littermates with myelin oligodendrocyte glycoprotein peptide 35-55. C3(-/-) mice were susceptible to EAE as much as the C3(+/+) mice were. No differences were found for the production of IL-2, IL-4, IL-12, TNF-alpha, and IFN-gamma between C3(+/+) and C3(-/-) mice. This finding shows that C3, a key component in C activation, is not essential in myelin oligodendrocyte glycoprotein peptide-induced EAE in mice.

publication date

  • January 15, 2001

Research

keywords

  • Complement Activation
  • Complement C3
  • Encephalomyelitis, Autoimmune, Experimental
  • Myelin-Associated Glycoprotein
  • Peptide Fragments

Identity

Scopus Document Identifier

  • 0035863728

Digital Object Identifier (DOI)

  • 10.4049/jimmunol.166.2.723

PubMed ID

  • 11145641

Additional Document Info

volume

  • 166

issue

  • 2