Experimental autoimmune encephalomyelitis is a model of multiple sclerosis induced in susceptible animals by immunization by intact myelin or components of myelin, the sheats that surrounds certain neurons. Like collagen induced arthritis for rheumatoid arthritis, experimental autoimmune encephalomyelitis can be induced in several species, including mice, rats, guinea pigs, rabbits, and primates. Although induced by heterologous antigens, the disease is autoimmune. Several proteins have been used to induce experimental autoimmune encephalomyelitis, including MBP, proteolipid protein (PLP), and MOG. Different antigens cause somewhat different clinical manifestations. By administering the antigen with complete Freund’s adjuvant and pertusis toxin, the blood-brain barrier is disrupted, permitting access by immune cells. The resulting demyelinating disease closely resembles human multiple sclerosis and is thought to be mediated primarily by T cells because disease can be transferred to normal animals by T cells (type IV autoimmune reactions). There is only limited evidence that an immune response to MBP, PLP or MOG is involved in human disease, and it is hypothesized that other myelin antigens may be the targets of autoreactive T cells in multiple sclerosis.