The pathogenesis and therapy of multiple sclerosis is based upon the requirement of a combination of myelin antigens for autoimmune demyelination.

It is postulated that the pathogenesis of demyelination in multiple sclerosis (MS) might lie in the cooperative effect of a T cell response against one myelin antigen (e.g. myelin basic protein--MBP) and a B cell response against a second myelin component which may act as a hapten or a carrier for the primary antigen. The hypothesis is based upon recent experiments in guinea pigs in which the encephalitogenicity of MBP was enhanced by the myelin glycolipid, galactocerebroside. This pathogenetic mechanism might be analogous to antibody-dependent, cell-mediated demyelination. Based upon this assumption, therapeutic trials in MS should take into consideration the possibility that instead of MBP alone, MBP might be more effective in combination with a lipid hapten.