Immunomodulation of experimental autoimmune uveitis using a rat anti retinal S-antigen specific monoclonal antibody: evidence for a species difference.

Experimental Autoimmune Uveitis (EAU) induced by retinal antigens, particularly S-antigen, forms a useful model of human chronic intraocular inflammation particularly endogenous posterior uveitis. It provides a means of assessing the efficacy of various agents used in the control of such inflammation. We induced an autoimmune uveitis and its associated pinealitis in Dunkin-Hartley guinea pigs and Lewis rats by inoculating them with bovine retinal S-antigen. In rats, induction of EAU but not of Experimental Autoimmune Pinealitis (EAP) could be prevented by the administration of S-antigen specific rat monoclonal antibody simultaneously with the S-antigen. Inhibition of EAU was accompanied by significantly raised levels of anti-S antibodies during the first two weeks post-immunisation. In contrast, the same monoclonal antibody failed to inhibit both EAU and EAP in guinea pigs. Immunocytochemical staining of rat tissues for lymphocyte subsets, monocytes and macrophages showed that eyes of monoclonal antibody treated animals contained no immunocompetent inflammatory cells unless they also had clinical signs of inflammation. In contrast, the inflammatory exudate in the pineal glands of both treated and untreated animals contained equal numbers of infiltrating lymphocytes and monocytes in the same relative proportions. These results indicate that the inhibitory effect of the monoclonal antibody S2.4.C5 is directed towards the effector arm of the immune-mediated cytotoxic response. A possible mechanism by which the antibody may be preferentially inhibiting the inflammatory response in the eyes but not in the pineal glands of rats, is suggested.