Loss of anterior chamber-associated immune deviation (ACAID) in aged retinal degeneration (rd) mice

PURPOSE. TO determine whether the capacity to induce ACAID by antigen injec tion into the anterior chamber is altered in animals with genetically deter mined retinal degeneration and increased age. METHODS. Anterior chamber-associated immune deviation (ACAID) induced by in jection of ovalbumin into the anterior chamber of the eye was studied in th ree rodent strains with different forms of hereditary retinal degeneration (Royal College of Surgeon [RCS] rats, retinal degeneration [rd] mice, and N orrie-Disease [ND] mice) and in different age groups (age range, 1-23 month s). The data were compared with those of age-matched controls. Aqueous humo rs of rd mice, RCS rats, and age-matched congenic controls were investigate d for concentrations of transforming growth factor-beta 2 (TGF-beta 2) usin g enzyme-linked immunosorbent assay. RESULTS. ACAID was readily induced in RCS rats and ND mice irrespective of amount of retinal degeneration or aging. In rd mice ACAID could be induced in young animals but not in animals more than 12 months of age. In old rd m ice, loss of ACAID was accompanied by a marked reduction in total TGF-beta 2 levels in aqueous humor. CONCLUSIONS. Rd mice more than 1 year of age lose the capacity of the anter ior chamber to support the induction of ACAID by intracameral injection of soluble protein antigen. Because loss of ACAID correlated with a decrease i n TGF-beta 2 concentration in aqueous humor, it is proposed that eyes of rd mice are unable to maintain an immunosuppressive microenvironment necessar y for ACAID.