In rodents, antibodies directed against the myelin component, myelin oligodendrocyte glycoprotein (MOG), are capable of opsonizing antigen [23] in the periphery and thereby trigger its uptake, presentation and subsequent activation of encephalitogenic T cells, resulting in experimental autoimmune encephalomyelitis (EAE) [24], an animal model for CNS demyelinating disorders. This evidence concerns the gene MOG and experimental autoimmune encephalomyelitis.