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MD Trousdale, D Stevenson, Z Zhu, JE Schechter, T Ritter, R Atkinson, AK Mircheff; Suppresses Lacrimal Gland Immunopathology and Ocular Surface Disease in a Rabbit Model of Autoimmune Dacryoadenitis . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3122.
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Purpose:To evaluate the effect of TNF-inhibitor gene expression on lacrimal gland immunopathology and ocular surface disease resulting from induced dacryoadenitis. Methods:Autoimmune dacryoadenitis was induced by injecting lacrimal gland with activated peripheral blood lymphocytes that had been cultured with autologous acinar cells (AMCR stimulated PBLs). In the treated group, adenovector carrying the TNF-inhibitor gene (AdTNFRp55-Ig, 1108 pfu) was injected concurrently with AMCR stimulated PBLs. Tear production was monitored by Schirmer test for 2 weeks, and tears were collected to examine TNF-inhibitor gene expression. Frozen sections of the gland were immunostained for rabbit thymic lymphocyte antigen (RTLA), CD18, and MHC-II. Results:TNF-inhibitor was detectable by ELISA in tears of the transduced animals. TNF-inhibitor titers peaked on day 3 and declined by day 7. Schirmer scores declined in the induced dacryoadenitis group, but not in the AdTNFRp55-Ig treated animals. By day 14, non-transduced glands had developed focal mononuclear cell infiltrates. RTLA, CD18 and MHC-II positive cells were significantly increased in the induced dacryoadenitis group. TNF-inhibitor treatment reduced the inflammatory infiltrates by 40% compared to dacryoadenitis group. Conclusion:In vivo transduction of the lacrimal gland with AdTNFRIp55-Ig resulted in transient expression in the gland and appearance of the TNF-inhibitor in tears. The TNF-inhibitor appeared to suppress the appearance of Sjögren’s syndrome-like features of reduced tear production and immunohistopathology associated with our experimental model of induced autoimmune dacryoadenitis.
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