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Terry Coursey, Stephen Pflugfelder, Cintia De Paiva; Upregulation of chemokine expression in experimental dry eye requires IL-17A and IFN-γ but not T cells. Invest. Ophthalmol. Vis. Sci. 2013;54(15):971.
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The chemokines CCL20 (CCR6 ligand), and CXCL-9, -10, -11 (CXCR3 ligands) coordinates migration of CCR6+Th17 cells and CXCR3+Th1 cells, respectively. Our previous studies have demonstrated the requirement of Th17 and Th1 cells in the pathogenesis of dry eye disease. The objective of this study was to evaluate the role of T cells (specifically Th1 and Th17 cells) in the upregulation of chemokine expression in an experimental model of dry eye.
Desiccating stress (DS) was induced by subcutaneous injection of scopolamine and exposure to a drafty low humidity environment in RAG1KO, IL-17KO, IFN-γKO and wild-type (WT) mice, aged 6-8 weeks for 5 or 10 days (DS5, DS10) or were not treated. CCL20, CXCL-9, CXCL-10, and CXCL-11 expression in the cornea and conjunctiva were evaluated by real time quantitative PCR.
Significant upregulation of CCL20 was observed in WT (> 30 fold) and RAG1KO (>7 fold) mice, however it was not upregulated in IFN-γKO mice and was significantly reduced in IL-17AKO mice (~2 fold). Similarly, CXCR3 ligands CXCL10 and -11 expression increased in WT (CXCL10- ~2 fold; CXCL11- ~2 fold) and RAG1KO (CXCL10- ~ 2 fold; CXCL11 ~ 2 fold) mice but not IFN-γKO or IL-17KO mice. CXCL9 was upregulated in WT mice (~5 fold) but not T cell deficient, IFN-γKO, or IL-17KO mice.
Upregulation of chemokine expression in experimental dry eye requires IL-17A and IFN-γ , but not T cells. Thus, exposure to DS induces the production of IL-17 and IFN-γ independent of the adaptive immune response.
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