Uveitis of unknown etiology is known to occur in association with various systemic disorders. We now report that anterior uveitis (AU) can be produced by T cell immunity to myelin basic protein (BP) and accompanies experimental autoimmune encephalomyelitis (EAE). EAE with AU was induced in Lewis rats by immunization to BP in CFA or by immunization to various BP peptides including the encephalitogenic 71-90 peptide. Slit-lamp biomicroscopy of BP-immunized Lewis rats revealed AU, characterised by inflammation of the iris, in 73% of the eyes. The onset of AU in actively immunized rats varied between days 12 and 26, often appearing after spontaneous remission of the paralysis, the hallmark of EAE. The course of AU was progressive, affecting more than 50% of the surface of the iris in 16 of 29 diseased eyes. Like the paralysis, the AU was self-limiting: within 2 weeks the disease remitted. In addition, AU could be adoptively transferred to naive and irradiated rats by a T cell clone specific for BP peptide 71-90. The present observations are compatible with the idea that AU may be triggered by BP-reactive T cells. The myelinated nerves present in the iris have been shown to contain BP. However, these peripheral nerves would now appear to be the only peripheral nerves susceptible to acute EAE.