Basic and clinical immunology in uveitis.

Understanding the basic immune mechanisms and how they relate to the eye are becoming obtainable goals with far reaching implications. Attempts are made to classically divide the immune responses noted into Type I-IgE mediated, Type II-Antibody mediated killing, Type III-Immune complex mediation, and Type IV-Cell mediated. Though several mechanisms are surely working simultaneously, it remains an helpful method of analysis. Until recently, Type III hypersensitivity reactions were thought to be the basic underlying cause of most ocular inflammatory disease, but recent evidence would suggest that cell mediated mechanisms are more important for sight threatening ocular disease (uveitis). The S-antigen and IRBP induced experimental models for uveitis have provided us with invaluable information concerning the potential mechanisms underpinning uveitis, while the diseases themselves manifest many aspects of that seen in human disease. Additionally, it has permitted us to investigate the way in which immune cells may "home" to a target organ, this in part due to the expression of HLA antigens on non-immune tissues in the eye. The observation that T-cell mechanisms appear of major import in uveitis permitted a new approach to therapy, the use of the anti-T-cell drug cyclosporine. Its use in severe sight threatening disease has shown it to be effective, thereby confirming the notion of the importance of T-cell mediation of these diseases. Perhaps most notable is this agent's efficacy in the treatment of Behçet uveitis. The problem of renal toxicity has been addressed by using cyclosporine in combination with other agents, including those not directly affecting the immune system.(ABSTRACT TRUNCATED AT 250 WORDS)