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Fig. 5 | BMC Ophthalmology

Fig. 5

From: Differential distribution of steroid hormone signaling networks in the human choroid-retinal pigment epithelial complex

Fig. 5

The GILZ protein is an immune-modulating protein that exerts numerous effects. GILZ inactivates several, transcription factors that regulate T-cell activation and differentiation, including NF-kB [21, 27]. GILZ was also shown to reduce Th1 transcription factor activity and activates Th2 transcription factors in T-cells from GILZ transgenic mice [28]. GILZ was shown to suppress lipopolysaccharide (LPS)-induced expression of several interleukins and chemokines in the retina in male Sprague-Dawley rats with endotoxin-induced uveitis [29]. Suppression of these cytokines inhibited macrophage Inflammatory protein-1 alpha (MIP-1a) which is expressed in the hypoxic inner retina in a C57BL/6 model for ischemia-induced retina neovascularization and may attract microglia that induce angiogenesis, suppressed monocyte chemoattractant protein-1 activity which has also been shown to mediate retinal neovascularization, and as well as supressed interleukin-beta [30,32,33,34]. GILZ suppresses dendritic cell (DC) activation markers and promoted tolerance markers, inhibiting T-cell activation and differentiation [21, 35, 36]. Finally, GILZ has been shown to inhibit interleukin 17 alpha production and subsequent activation of Th17 cells in a murine model for streptozotocin-induced diabetes which increases retinal inflammation [37]. Pie charts adjacent to proteins represent the protein’s relative abundance in the periphery (blue), macula (orange), and fovea (gray) based on the mass spectrometry data provided by the Skeie and Mahajan [5] study

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