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A. Amadi-Obi, C.-R. Yu, Y. Lee, R. M. Mahdi, C. E. Egwuagu; IL-27 Secreted by Retinal Microglia Induces IL-10 Expression in Retinal Cells. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2643.
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Ocular immune privilege is actively maintained by multiple factors, including neuropeptides such as -MSH and cytokines such as TGFβII. We recently showed that IL-27, an IL-12 family cytokine with anti-inflammatory properties, is constitutively expressed in the retina. In this study we sought to characterize the cell types in the neuroretina that secrete IL-27 and whether IL-27 contributes to ocular immune privilege by inducing the expression of immunosuppressive proteins.
For localization of IL-27 expression in the retina, sections from normal mouse retina were stained with IL27p28, EBI3, IL27 receptor and F4/80 (microglia cell marker) antibodies. To examine effects of IL27 primary retinal cells isolated from several mouse strains were cultured with IL-27 and its effects on gene expression were analyzed by RT-PCR, qRT-PCR and Western blotting.
Expression of IL27p28 and EBI3 localizes to ganglion and inner nuclear layers of the retina. IL-27p28 also co-localizes with F4/80,a surface marker for microglia cells.We further show that resident retinal cells express the IL-27 receptor and stimulation with IL-27 activates STAT1 and leads to expression of the anti-inflammatory cytokine Interleukin-10. Expression of suppressor of cytokine signaling protein 1 (SOCS1) and SOCS3 was also induced and both proteins play essential roles in mitigating pathogenic effects of pro-inflammatory cytokines. We further show that these effects of IL-27 on gene expression are abrogated in STAT1-/- mice
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