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

Jerry Y. Niederkorn^2,3,*, Michael E. Stern^2,, Stephen C. Pflugfelder^2,, Cintia S. De Paiva, Rosa M. Corrales, Jianping Gao and Karyn Siemasko

^* Department of Ophthalmology, University of Texas Southwestern Medical Center, Dallas, TX 75390; Department of Biological Sciences, Allergan, Irvine, CA 92623; and 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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The JI 2006 176: 3851-3852. [Full Text]  

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