Loss of Anterior Chamber-Associated Immune Deviation (ACAID) in Aged Retinal Degeneration (rd) Mice

• Published in: Investigative ophthalmology & visual science Vol. 40; no. 13; pp. 3209 - 3214
• Main Authors: Welge-Lu{beta}en, Ulrich, Wilsch, Caren, Neuhardt, Thomas, Streilein, J. Wayne, Lutjen-Drecoll, Elke
• Format: Journal Article
• Language: English
• Published: Rockville, MD ARVO 01.12.1999; Association for Research in Vision and Ophtalmology
• Subjects: Aging - immunology; Animals; Anterior Chamber - immunology; Anterior Chamber - metabolism; Aqueous Humor - metabolism; Biological and medical sciences; Enzyme-Linked Immunosorbent Assay; Eye Diseases, Hereditary - genetics; Eye Diseases, Hereditary - immunology; Eye Diseases, Hereditary - metabolism; Medical sciences; Mice; Mice, Inbred C57BL; Mice, Mutant Strains; Ophthalmology; Ovalbumin - immunology; Rats; Rats, Mutant Strains; Retinal Degeneration - genetics; Retinal Degeneration - immunology; Retinal Degeneration - metabolism; Retinopathies; Transforming Growth Factor beta - metabolism; Animal model; Retinopathy; Transforming growth factor β; Pathogenesis; Rodentia; Concentration; Aqueous humor; Hereditary; Genetic disease; Eye; Eye disease; Vertebrata; Mammalia; Mouse; Animal; Anterior chamber; Immune deviation; Age
• ISSN: 0146-0404; 1552-5783

To determine whether the capacity to induce ACAID by antigen injection into the anterior chamber is altered in animals with genetically determined retinal degeneration and increased age. Anterior chamber-associated immune deviation (ACAID) induced by injection of ovalbumin into the anterior chamber of the eye was studied in three rodent strains with different forms of hereditary retinal degeneration (Royal College of Surgeon [RCS] rats, retinal degeneration [rd] mice, and Norrie-Disease [ND] mice) and in different age groups (age range, 1-23 months). The data were compared with those of age-matched controls. Aqueous humors of rd mice, RCS rats, and age-matched congenic controls were investigated for concentrations of transforming growth factor-beta2 (TGF-beta2) using enzyme-linked immunosorbent assay. 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 mice, loss of ACAID was accompanied by a marked reduction in total TGF-beta2 levels in aqueous humor. Rd mice more than 1 year of age lose the capacity of the anterior chamber to support the induction of ACAID by intracameral injection of soluble protein antigen. Because loss of ACAID correlated with a decrease in TGF-beta2 concentration in aqueous humor, it is proposed that eyes of rd mice are unable to maintain an immunosuppressive microenvironment necessary for ACAID.