December 2002
Volume 43, Issue 13
Free
ARVO Annual Meeting Abstract  |   December 2002
Lacrimal Gland Immonopathology and Ocular Surface Disease in a Rabbit Model of Autoimmune Dacryoadenitis
Author Affiliations & Notes
  • Z Zhu
    Doheny Eye Institute and Department of Ophthalmology Los Angeles CA
  • D Stevenson
    Doheny Eye Institute and Department of Ophthalmology Los Angeles CA
  • JE Schechter
    Department of Cell & Neurobiology
    Keck School of Medicine University of Southern California Los Angeles CA
  • AK Mircheff
    Doheny Eye Institute and Deparments of Ophthalmology Physiology & Biophysics Keck School of Medicine University of Southern California Los Angeles CA
  • R Atkinson
    Department of Pathology
    Keck School of Medicine University of Southern California Los Angeles CA
  • MD Trousdale
    Doheny Eye Institute and Department of Ophthalmology Keck School of Medicine University of Southern California Los Angeles CA
  • Footnotes
    Commercial Relationships   Z. Zhu, None; D. Stevenson, None; J.E. Schechter, None; A.K. Mircheff, None; R. Atkinson, None; M.D. Trousdale, None. Grant Identification: Supported by EY12689, EY05801, EY10550, EY03040, grants from RPB and Allergan.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 3121. doi:
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      Z Zhu, D Stevenson, JE Schechter, AK Mircheff, R Atkinson, MD Trousdale; Lacrimal Gland Immonopathology and Ocular Surface Disease in a Rabbit Model of Autoimmune Dacryoadenitis . Invest. Ophthalmol. Vis. Sci. 2002;43(13):3121.

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Abstract

Abstract: : Purpose: To study the manifestations of lacrimal immunopathology and ocular surface disease in a recently developed rabbit model of autoimmune dacryoadenitis. Methods: Rabbit lacrimal glands were injected with peripheral blood lymphocytes (PBLs) that were pre-stimulated in an autologous mixed cell reaction (AMCR) with purified acinar cells. Rabbits with lacrimal glands inoculated with non-stimulated PBLs, unilateral lacrimal gland excised, or no treatment were examined as controls. Eyes were monitored for clinical manifestations of disease biweekly for 8 weeks. Lacrimal glands were then removed and frozen sections immunostained for MHC II, CD4, CD8, CD18 and rabbit thymic lymphocyte antigen (RTLA). Relative numbers of positively stained cells were quantitated with Chromavision image analysis system. Results: Tear production (measured by Schirmer test) and tear break-up time (BUT) decreased with a concomitant increase of the rose bengal score in both AMCR-PBL injected eyes and the contralateral, non-injected eyes. No obvious changes were found in the non-stimulated PBL injected group. In unilateral lacrimal gland removal group, there was a marked decrease of tear production and BUT and an increase in rose bengal staining during the first two weeks with a gradual recovery at 8 weeks. Interstitial cells in normal lacrimal glands expressed CD18 and RTLA, but few expressed CD4, CD8 or MHC II. Characteristic focal mononuclear cell infiltrates were only found in lacrimal glands receiving AMCR-PBLs and were predominantly CD4+ T cells. MHC II, RTLA, CD18 and CD8 were also significantly increased compared to controls. Conclusion: Injection of AMCR-PBLs into the lacrimal gland induces autoimmune dacryoadenitis with immunopathological features similar to Sjögren’s syndrome. The lacrimal immunopathology is accompanied by typical clinical manifestations of dry eye syndrome.

Keywords: 376 cornea: tears/tear film/dry eye • 327 autoimmune disease • 452 lacrimal gland 
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