The observations that incubation of IRBP-specific T cells with RACs pre-exposed to BLP plus NOD2 led to the production of higher levels of IFN-γ and IL-17 by IRBP1-20-specific T cells and that adoptive transfer of these cells into naïve mice induced severe uveitis suggests that the stimulation of RACs via both the NOD2 and TLR2 pathways is a more potent inducer of the APC function of RACs than either ligand alone and that a variety of infectious pathogens may have the ability to stimulate RACs and contribute to the development of autoimmune uveitis. This evidence concerns the gene NOD2 and autoimmune uveitis.