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

  • Calida D
  • Constantinescu C
  • Purev E
  • et al.
68Citations
Citations of this article
17Readers
Mendeley users who have this article in their library.

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-α, and IFN-γ, 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.

Cite

CITATION STYLE

APA

Calida, D. M., Constantinescu, C., Purev, E., Zhang, G.-X., Ventura, E. S., Lavi, E., & Rostami, A. (2001). 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. The Journal of Immunology, 166(2), 723–726. https://doi.org/10.4049/jimmunol.166.2.723

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free