ANTIBODY FACILITATION OF MULTIPLE SCLEROSIS-LIKE LESIONS IN A NONHUMAN PRIMATE

In the human disease multiple sclerosis (MS), the immune mechanisms re sponsible for selective destruction of central nervous system myelin a re unknown, In the common marmoset Callithrix jacchus, a unique demyel inating form of experimental allergic encephalomyelitis resembling MS can be induced by immunization with whole myelin. Here we show that th e MS-like lesion can be reproduced by immunization against the extrace llular domain of a single myelin protein, myelin/oligodendrocyte glyco protein (MOG), By contrast, immunization against the quantitatively ma jor myelin proteins myelin basic protein or proteolipid protein result s in inflammation but little or no demyelination, Furthermore, in the presence of encephalitogenic (e,g,, disease-inducing) T cells, the ful ly demyelinated lesion is reconstructed by systemic administration of IgG purified from whole myelin-, or MOG-immunized animals, and equally by a monoclonal antibody against MOG, but not by control IgG, Encepha litogenic T cells may contribute to the MS-like lesion through disrupt ion of the blood brain barrier that permits access of demyelinating an tibody into the nervous system, The identification of MOG as a major t arget antigen for autoimmune demyelination in a nonhuman primate shoul d facilitate development of specific immunotherapies for human MS.