Multiple sclerosis and experimental autoimmune encephalomyelitis

Multiple sclerosis (MS) is the most frequent of demyelinating diseases of the central nervous system (CNS). Its cause is unknown, but it has been clearly established that environmental and genetic factors contribute to its genesis. The resemblance between the anatomico-pathological features of MS and those of an experimental model, experimental autoimmune encephalomyelitis (EAE), reinforced by the presence of immune abnormalities in the cerebrospinal fluid and blood of MS patients, strongly suggests that an autoimmune process participates in MS. In genetically susceptible animals EAE is induced by myelin antigens. The disease can be transferred by autoimmune myelin basic protein specific T cells which migrate into the cerebrospinal fluid through the blood-brain barrier. Studies of fine specificity antigenic recognition, restriction by molecules from the major histocompatibility complex (MHC), T-receptor and functional properties of T cells have made it possible to devise highly specific immunotherapies aimed at preventing the activation phase and the effector phase of autoimmune cells. Selective inhibition of EAE is obtained by vaccination with attenuated autoimmune T cells, by immunotoxins, by monoclonal antibodies directed against molecules expressed at the T cell membrane, by synthetic T-receptor peptides, by a copolymer cross reacting with the myelin basic protein or by oral administration of the myelin basic protein itself. Some of these immunotherapies are transposed to MS.