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Desiccating stress induces T cell-mediated Sjögren's Syndrome-like lacrimal keratoconjunctivitis.

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.[1]

References

  1. Desiccating stress induces T cell-mediated Sjögren's Syndrome-like lacrimal keratoconjunctivitis. Niederkorn, J.Y., Stern, M.E., Pflugfelder, S.C., De Paiva, C.S., Corrales, R.M., Gao, J., Siemasko, K. J. Immunol. (2006) [Pubmed]
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