Autoantibody-mediated demyelination depends on complement activation but not activatory Fc-receptors.

ABSTRACT: The precise mechanisms leading to CNS inflammation and myelin destruction in both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) remain the subject of intense debate. In both MS and EAE, autoantibodies (autoAbs) are thought to be involved in tissue destruction through recruiting Fc receptor (FcR)-bearing cells or direct cytotoxic effects through the activation of the complement pathway. Whereas intrathecal immunoglobulin (Ig) production and Ig deposition in inflammatory lesions is a hallmark of MS, mice deficient in B cells and Igs develop severe EAE. Paradoxically, mice of the same genetic background but deficient in FcRgamma are EAE-resistant. We found that the functional expression of FcRgamma on systemic accessory cells, but not CNS-resident cells, appears

SUBMITTER: Urich E 

PROVIDER: S-EPMC1693725 | biostudies-literature | 2006 Dec

REPOSITORIES: biostudies-literature