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Ulrich Welge–Lüßen, Caren Wilsch, Thomas Neuhardt, J. Wayne Streilein, Elke Lütjen–Drecoll; Loss of Anterior Chamber-Associated Immune Deviation (ACAID) in Aged Retinal Degeneration (rd) Mice. Invest. Ophthalmol. Vis. Sci. 1999;40(13):3209-3214.
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purpose. 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.
methods. 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-β2 (TGF-β2) using
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 mice, loss of ACAID was accompanied by a marked reduction in
total TGF-β2 levels in aqueous humor.
conclusions. 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-β2 concentration in aqueous humor, it is proposed
that eyes of rd mice are unable to maintain an immunosuppressive
microenvironment necessary for ACAID.
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