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Y. Ke, D. Sun, G. Jiang, Y. Bian, H. J. Kaplan, H. Shao; Exposure of Retinal Astrocytes to IL-17 Elicited Massive Expression of Cytokines and Chemokines That Recruit Non Lymphoid Inflammatory Cells. Invest. Ophthalmol. Vis. Sci. 2008;49(13):2528.
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We have previously shown that autoreactive IL-17 producing T cells could induce experimental autoimmune uveitis (EAU). However, the mechanisms of IL-17 in the pathogenic events of uveitis are largely unknown. To determine the pathogenic events induced by IL-17, we have examined the effect of IL-17 on the parenchymal cells of the retinal astrocytes and RPE.
Retinal astrocytes and RPE were isolated as we previously reported. The cells were exposed to graded doses of IL-17. The cytokine/chemokines in the supernatants of astrocytes and RPE were examined by ELISA. The chemotaxis of the supernatants to the migration of T cells, granulocytes, or monocytes/macrophages was determined. Signal transduction pathways involved in the interaction of IL-17 and IL-17R on these cells were examined.
Both RACs and RPE express IL-17 receptor; however, only astrocytes vigorously responded to IL-17 by producing increased amounts of cytokines and chemokines, which promoted the migration of granulocytes, monocytes and macrophages, but not T cells. The interaction of IL-17/IL-17R on RACs is mainly dependent on PI-3K/AKT signaling pathway.
IL-17 produced by the IL-17+ IRBP-specific T cells can activate local parenchymal cells such as astrocytes and activated astrocytes release abundant amounts of cytokines and chemokines, which recruit non-lymphoid inflammatory cells, in turn, amplify inflammatory cascades in the eye.
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