ABSTRACT
A large body of immunologic, epidemiologic, and genetic data indicate that tissue injury in multiple sclerosis (MS) results from an abnormal (i.e. autoimmune) inflammatory response to one or more myelin antigens, a response that is probably triggered by an environmental exposure in a genetically susceptible host. The inflammatory changes that occur in MS may ultimately be shown to be secondary rather than primary, and only tentative assumptions of the nature of MS can be reasonably made at this time. Indeed, inflammation and selective destruction of central nervous system (CNS) elements may also occur in non-autoimmune conditions; such diseases of known etiology include genetic disorders (adrenoleukodystrophy, metachromatic leuko dystrophy) and chronic virus infections with human T cell leukemia virus (HTLV)-l and Theiler murine encephalomyelitis virus.
