ACTIVE AND PASSIVELY INDUCED EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS IN COMMON MARMOSETS - A NEW MODEL FOR MULTIPLE-SCLEROSIS

A chronic relapsing-remitting form of experimental autoimmune encephal omyelitis was induced in the common marmoset Callithrix jacchus follow ing a single immunization with human white matter. Individual animals in this species are born as natural bone marrow chimeras, allowing tra nsfer of functional T-cell populations between genetically distinct si blings. The acute disease was characterized clinically by mild neurolo gical signs. Pathologically, the disease was characterized by perivasc ular mononuclear cell infiltrates, large foci of primary demyelination , and reactive astrogliosis. No animal displayed hemorrhagic-necrotic lesions or polymorphonuclear cell infiltrates characteristic of other acute forms of primate experimental autoimmune encephalomyelitis. A la te spontaneous relapse occurred in each of 2 animals followed for 3 to 12 months subsequent to recovery from the acute attack. In these anim als, chronic lesions consisted of mononuclear cell infiltrates within large sharply defined areas of demyelination and astrogliosis, and res embled active plaques of chronic multiple sclerosis. Proliferative res ponses to myelin basic protein but not to myelin proteolipid protein w ere present in peripheral blood lymphocytes df immunized animals. Furt hermore, myelin basic protein-reactive T-cell lines derived from immun ized donors induced clinical signs of experimental autoimmune encephal omyelitis when adoptively transferred into a sibling, indicating that myelin basic protein-reactive T cells can induce disease in this speci es. Because of its clinical and pathological similarity to human multi ple sclerosis and the ability to adoptively transfer experimental auto immune encephalomyelitis, this model system should prove useful in the analysis of the immunological mechanisms responsible for autoimmune d emyelination in outbred primates.