OBJECTIVE Intercellular adhesion molecule-1 (ICAM-1), which is one of the ligands for lymphocyte function associated antigen-1 (LFA-1), plays an important role in immune responses. To examine whether ICAM-1 and LFA-1 are involved in the pathogenesis of experimental autoimmune uveoretinitis (EAU), the authors investigated the therapeutic effect of anti-ICAM-1 monoclonal antibody (mAb) 1A29 and anti-LFA-1 alpha chain mAb WT.1 on retinal soluble antigen (S-Ag) and Freund's complete adjuvant (FCA)-induced EAU in rats. METHODS After immunization with S-Ag and FCA, rats were intraperitoneally injected with a monoclonal antibody, anti-ICAM-1 mAb 1A29 or anti-LFA-1 alpha chain mAb or control Ab, at 1.0 mg/kg body weight, according to the treatment schedule. Inflammation was examined clinically and histologically. Proliferative responses of splenocytes to S-Ag were also examined. RESULTS The development of EAU could be completely prevented by the administration of 1A29, 1.0 mg/kg, twice a week from day 0 to day 14, but was only partially suppressed by WT.1. However, semiweekly administration of 1A29 from day 0 to day 7, or from day 10 to day 17, did not suppress EAU. CONCLUSIONS These findings indicate that ICAM-1, LFA-1-dependent pathways are involved in the pathogenesis of EAU. In addition, these pathways seem to be required for both the induction and the development of this disease.