Immunoregulatory mechanisms in experimental autoimmune uveitis : the role of major histocompatibility complex products, retinal pigment epithelial cells and mononuclear leucocytes
In this study a possible role for RPE cells as local antigen presenting cells in immune inflammatory eye disease was investigated. In contrast to observations in the rat model of EAU however, Class II positive RPE cells were never observed in vivo in the guinea pig model of EAU but responses of RPE cells in vitro implied that these cells may have an immunoregulatory role in retinal autoimmunity. The T cell mediated nature of EAU was studied in the guinea pig model. The phenotype of inflammatory cells present in developing lesions was examined. Earliest choroidal infiltrates appeared to be Th cells, but in established choroidal foci of inflammatory cells and in early retinal lesions, where rod outer segment (ROS) lysis was occurring, the presence of a Pan T-ve, Tc/s+ve population of putative effector cells was identified. In endstage lesions B cells became the predominant cell type, and may act as suppressor cells in this species. Infiltrating inflammatory cells and capillary endothelial cells expressed Class I and Class II antigens but RPE and Muller cells did not. Cyclosporin A (CsA) therapy prevented vitreal inflammation and there was a marked reduction of Class II antigen expression despite choroidal infiltrates of Tc/s. Delayed type hypersensitivity (DTH) skin reactions to retinal antigen were also profoundly suppressed by CsA.