These results, together with previous reports by ourselves and others showing that complement components accumulated adjacent to sites of inflammation in EAU (35), that C3 KO mice (21) and C3aR/C5aR KO mice (23) develop less severe EAU than WT mice, and that treating WT mice with complement inhibitors, such as recombinant DAF (22), soluble Crry (21), or an anti-C5 mAb (36), reduces the severity of EAU, confirm a critical role of the complement system in the pathogenesis of EAU and raise the possibility that it may influence its human counterpart, autoimmune uveitis. This evidence concerns the gene CD55 and autoimmune uveitis.