The aim of this study was to explore whether IL-7 participates in the pathogenesis of Graves' ophthalmopathy (GO). This was a prospective study. 20 GO patients (40 eyes) and 20 healthy volunteers (40 eyes) were recruited. The tear concentration of IL-7 was measured using ELISA assay. IL-7 expression in orbital tissues was evaluated by immunohistochemistry. Patients with inactive GO had the highest IL-7 concentrations in the tears, followed by healthy controls and patients with active GO per ELISA. Immunohistochemistry analysis showed that IL-7 expression in orbital tissues of the inactive GO samples was higher than that of the volunteers. Changes of IL-7 expression in different phases of GO suggested that IL-7 may play an important role in the pathogenesis of GO.

Background. Uveal melanoma (UM) has favorable local tumor control, but once metastasis develops, the prognosis is rather poor. Thus, it is urgent to develop metastasis predicting markers. Objective. Our study investigated a novel gene expression-based signature in predicting metastasis for patients with UM. Methods. In the discovery phase, 63 patients with UM from GEO data set GSE22138 were analyzed using the Weighted Correlation Network Analysis (WGCNA) to identify metastasis-related hub genes. The Least Absolute Shrinkage and Selection Operator (Lasso) Cox regression was used to select candidate genes and build a gene expression signature. In the validation phase, the signature was validated in The Cancer Genome Atlas database. Results. Forty-one genes were identified as hub genes of metastasis by WGCNA. After the Lasso Cox regression analysis, eight genes including RPL10A, EIF1B, TIPARP, RPL15, SLC25A38, PHLDA1, TFDP2, and MEGF10 were highlighted as candidate predictors. The gene expression signature for UM (UMPS) could independently predict MFS by univariate and multivariate Cox regression analysis. Incorporating UMPS increased the AUC of the traditional clinical model. In the validation cohort, UMPS performed well in predicting the MFS of UM patients. Conclusions. UMPS, an eight-gene-based signature, is useful in predicting prognosis for patients with UM.

The monocyte adhesion to endothelial cells is an early step in chronic inflammation. Interferon-γ (IFN-γ) is regarded as a master regulator of inflammation development. However, the significance of IFN-γ in the monocyte adhesion to endothelial cells remains largely unknown. In this study, we found that IFN-γ increased PD-L1 transcription in endothelial cells through IRF-1 transcription factor, and subsequently enhanced the adhesion of monocyte to endothelial cells. PD-L1 in endothelial cells interacted with CD169/Siglec 1 in monocyte depending on the α2,3-sialylation of PD-L1. ST3Gal4 (ST3β-galactoside α-2,3-sialyltransferase 4) was the major glycosyltransferase responsible for the α2,3-sialylation of PD-L1. Down-regulation of α2,3-sialylation of PD-L1 by ST3Gal4 knockdown reduced the PD-L1-CD169 interaction. Purified PD-L1 protein with α2,3-sialylation, but not PD-L1 protein without α2,3-sialylation, reduced IFN-γ-induced monocytes adhesion to endothelial cells. Collectively, the interaction between PD-L1 and CD169 promoted monocytes adhesion to endothelial cells. Our findings provide a new mechanism of monocytes adhesion to endothelial cells.

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