The clinical, histological, and immunological features of experimental autoimmune uveo-retinitis (EAU) produced with purified retinal S antigen have been defined in several mammalian species. Further investigations of the model will focus upon mechanisms of the disease process. The available evidence has implicated involvement of the T-lymphocyte, although participation of immune complexes appears to be a factor in highly sensitized animals. The role of antigen-stimulated T-lymphocytes will be examined by passive transfer of peritoneal exudate lymphocytes obtained from sensitized inbred donor guinea pigs to normal animals of the same strain. Other studies will explore the role of preformed immune complexes injected systemically or intraocularly in pathogenesis. Still other investigations will examine EAU as a chronic disease and attempt to modulate the course of the disease by immune suppression. It is also planned to initiate experiments on the isolation and identification of U antigen, one of the three antigens originally implicated in pathogenesis of EAU.