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J. El Annan, S. K. Chauhan, T. Ecoiffier, D. R. Saban, Q. Zhang, R. Dana; Characterization of Effector T cells in Dessicating Stress-Induced Keratoconjunctivits Sicca. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3235. doi: https://doi.org/.
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Dry eye syndrome (DES), one of the most common indications for patients seeking ophthalmic care, is associated with T cell recruitment to the ocular surface, suggesting that it is an immune-mediated disorder. The purpose of these experiments was to characterize the phenotype of the T cells activated in DES in a preclinical murine model of dry eye.
Dry eye was induced in female C57BL/6 mice by exposure to a desiccating environment (relative humidity (RH) =22 ± 5%, airflow (AF) =15 L/min, temperature (T) = 21-23 oC) and to systemic scopolamine. Draining lymph nodes were harvested from dry eye and normal mice. The expression of T cell surface activation markers and chemokine receptors were analyzed by flow cytometry. T cell proliferation and cytokine secretion were detected by bromodeoxyuridine incorporation assay and ELISA respectively.
Draining lymph node (LN) T cells of dry eye mice expressed significantly higher levels of CD69 (p<0.05), and CCR5 (p<0.05). T cells from these LN showed a significant increase in IFN-γ (p<0.05) secretion, a decrease in IL-4 (p<0.05) secretion, and an increased proliferative capacity in response to CD3 stimulation.
The increased expression of cell surface activation markers, proliferation, and higher secretion of IFN-γ, but not IL-4, indicates that a T helper-1 (Th1) type immune response is generated in regional LN in DES. These data provide further support for the hypothesis that DES is an autoimmune disease characterized by a regional or systemic Th1 response.
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