July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Etiopathogeneses of Lacrimal Gland Autoimmune and Chronic Inflammatory Phenotypes
Author Affiliations & Notes
  • Austin K Mircheff
    Physiology & Neuroscience, University of Souther California, Los Angeles, California, United States
  • Footnotes
    Commercial Relationships   Austin Mircheff, None
  • Footnotes
    Support  NIH Grant EY017731
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 3286. doi:
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      Austin K Mircheff; Etiopathogeneses of Lacrimal Gland Autoimmune and Chronic Inflammatory Phenotypes. Invest. Ophthalmol. Vis. Sci. 2019;60(9):3286.

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      © ARVO (1962-2015); The Authors (2016-present)

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Presentation Description : Understanding the early steps in the pathogeneses of the inflammatory infiltrates that cause lacrimal gland secretory dysfunction and aqueous-deficient dry eye disease could lead to earlier diagnosis, earlier intervention, and better outcomes. The lymphocytic infiltrates may be focal and associated with autoantibody production, pathognomonic of Sjögren’s syndrome, or, as occurs much more frequently, they may be manifestations of chronic, immune-mediated inflammatory process that do not give rise to autoantibodies. Both types of lesion are heterogeneous. For example, Sjögren’s lesions can be dominated by T cells or by B cells, and the B cell-predominant lesions may have or lack germinal centers. We have used real time RT-PCR to assay immune response-related gene transcript expression in extracts of lacrimal glands from rabbits that experienced different environmental and hormonal exposures and in microdissected samples of infiltrating immune cells and of acini, intralobular ducts, interlobular ducts, and interlobar ducts from nulliparous rabbits and term-pregnant rabbits that experienced the same environmental exposure. Our findings indicate that epithelial cells and immune cells are actively communicating with each other in glands that are still histologically normal. The communication shapes gene expression in highly localized networks that comprise both epithelial cells and immune cells. Signals related to the dryness and temperature of the ambient environment and signals from the hormonal environment interact with localized stochastic phenomena to influence the networks’ cellular compositions and gene expression profiles. These findings suggest that epithelial cell-immune cell networks which may develop into autoimmune- or chronic, immune-mediated lesions of diverse phenotypes have already formed by the time of sexual maturity, if not earlier. That gene expression signatures of networks with various phenotypes can be detected in glands that are histologically normal should have important implications for the design of early diagnostic paradigms and proactive disease modifying therapies.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.


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