Evidence is now accumulating on both clinical and experimental grounds that the retina is an a priori source of inflammatory activity. Reactive inflammation in the retina may produce many of the clinical signs previously ascribed to uveal inflammation. Autoimmune mechanisms are probably responsible for the majority of cases of retinal vasculitis. Autoimmune retinal vasculitis occurs without other classical signs of inflammatory response in any other parts of the body. When associated systemic manifestations occur they may reflect different underlying immunopathogenic abnormalities. Thus in diseases with predominantly arterial involvement (e.g. systemic lupus erythematosus, polyarteritis nodosa) the retinal arteries bear the brunt of this disease. In Behçet's disease the systemic involvement is usually venous and ocular involvement produces diffuse capillary and venous inflammation with areas of retinal necrosis and major vascular occlusion. The retinal appearances differ from sarcoidosis in which a granulomatous response produces characteristic periphlebitis. Finally, autoimmune retinal vasculitis produces diffuse capillary and venous damage, without any systemic signs. In the next decade the search will be for the identification of the specific antigens initiating these disparate retinal features. Retinal S antigen is a potent antigen, but rhodopsin, interphotoreceptor binding protein, and transducin all need further experimental investigation. Precise documentation will herald the dawn of new therapeutic measures based on a sound immunological fabric.
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