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The Journal of Immunology, 2006, 176: 3950-3957.
Copyright © 2006 by The American Association of Immunologists

Desiccating Stress Induces T Cell-Mediated Sjögren’s Syndrome-Like Lacrimal Keratoconjunctivitis1

Jerry Y. Niederkorn2,3,*, Michael E. Stern2,{dagger}, Stephen C. Pflugfelder2,{ddagger}, Cintia S. De Paiva{ddagger}, Rosa M. Corrales{ddagger}, Jianping Gao{dagger} and Karyn Siemasko{dagger}

* Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX 75390; {dagger} Department of Biological Sciences, Allergan, Irvine, CA 92623; and {ddagger} Department of Ophthalmology, Baylor College of Medicine, Houston, TX 77030

Chronic dry eye syndrome affects over 10 million people in the United States; it is associated with inflammation of the lacrimal gland (LG) and in some cases involves T cell infiltration of the conjunctiva. We demonstrate that environmental desiccating stress (DS) elicits T cell-mediated inflammation of the cornea, conjunctiva, and LG, but not other organs in mice. The lacrimal keratoconjunctivitis (LKC) was mediated by CD4+ T cells, which, when adoptively transferred to T cell-deficient nude mice, produced inflammation in the LG, cornea, and conjunctiva, but not in any other organ. Adoptively transferred CD4+ T cells produced LKC even though recipients were not exposed to DS. LKC was exacerbated in euthymic mice depleted of CD4+CD25+forkhead/winged helix transcription factor+ regulatory T cells. The results suggest that DS exposes shared epitopes in the cornea, conjunctiva, and LG that induce pathogenic CD4+ T cells that produce LKC, which under normal circumstances is restrained by CD4+CD25+forkhead/winged helix transcription factor+ regulatory T cells.


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