 Glatiramer acetate has been shown to be a more general suppressor of autoimmune disease, inhibiting the onset of experimental animal models of uveoretinitis, rheumatoid arthritis, immune rejection of grafts against host and host against graft disease, and inflammatory bowel disease. Glatiramer acetate was originally developed based on the observation that it inhibited the onset of clinical disease in an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis EAE. Glatiramer acetate suppression of EAE was found to be a general phenomenon not restricted to a particular species, disease type or encephalitogen used for the induction of EAE. A unique feature of glatiramer acetate is its promiscuous binding with high affinity to various class II MHC molecules and it potent induction of Th2 regulatory T cells. Moreover glatiramer acetate has subsequently been shown to be a more general suppressor of autoimmune disease, inhibiting the onset of experimental uveoretinitis, immune rejection of grafts against host and host against graft disease, and experimental inflammatory bowel disease. 