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J. Mo, S.W. John, J.W. Streilein; Early Loss of Immune Privilege and Appearance of Immunogenic Inflammation Characterize Eyes of DBA/2J Mice with Pigmentary Glaucoma . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4304.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: A type of pigmentary glaucoma develops in genetically inbred DBA/2J mice that possess mutant genes causing iris stromal atrophy and iris pigment dispersion. Because pigment-laden macrophages are prominent in the anterior segments of affected DBA/2J eyes, and because one of the mutant genes (Gpnmb) is expressed in bone marrow-derived cells of the monocyte/dendritic cell lineage, the present study was designed to study the eyes of these mice for evidence of compromised immune privilege. Methods: AqH from eyes of DBA/2J mice of various ages was tested for presence of protein and leukocytes, and for its capacity to suppress T cell activation in vitro. Immune privilege and ACAID were assayed, respectively, following injection of histoincompatible, BALB/c-derived CT26.WT tumor cells or ovalbumin (OVA) into the anterior chamber. Results: AqH acquired elevated protein levels and leukocytes coincident with the first clinical evidence of pigment dispersion in the eyes of mice (between 4 and 6 months of age), indicating breakdown of the blood:ocular barrier. AqH from eyes of mice 2 mos and older failed to suppress T cell activation, and these eyes failed to support ACAID induction. Growth of allogeneic tumor cells implanted in the anterior chamber was delayed in eyes of 7 mos old mice. Conclusions: Immune privilege is compromised in eyes of mice with pigment dispersion, and evidence of this compromise precedes clinical signs of disease, implying a role for altered immune privilege and immunogenic inflammation in onset and pathogenesis of pigmentary glaucoma.
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