Interleukin (IL)-35 strongly suppresses the immune effects of CD8+ T cells. However, the mechanisms mediating these effects are not clear. Here, we investigated the potential inhibitory mechanisms of IL-35 using proteomics technology. The changes of differentially expressed proteins (DEPs) were evaluated using gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. IL-35 negatively regulated the expression of proteins in the biological processes category. GO analysis identified cellular immunosuppression regulation and external stimulation of regulatory proteins as pathways that were most affected by IL-35. Among the proteins regulated in these pathways, cell-matrix adhesion junction and anchoring junction proteins were more abundant. KEGG pathway analysis showed that cytochrome c and IL-12A were significantly altered. DEPs were related to cell signaling, migration, inhibition, apoptosis, and enrichment of arachidonic acid metabolism. These findings improved our understanding of the roles of IL-35 in inhibition of CD8+ T cells.

中文翻译：

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蛋白质组学分析揭示了影响CD8 + T细胞功能的白介素35依赖性调节机制。

白介素（IL）-35强烈抑制CD8 + T细胞的免疫作用。但是，介导这些作用的机制尚不清楚。在这里，我们使用蛋白质组学技术研究了IL-35的潜在抑制机制。使用基因本体论（GO）和《京都基因与基因组百科全书》（KEGG）途径分析评估了差异表达蛋白（DEPs）的变化。IL-35在生物过程类别中负调控蛋白质的表达。GO分析确定了细胞免疫抑制调节和调节蛋白的外部刺激是受IL-35影响最大的途径。在这些途径调节的蛋白质中，细胞-基质粘附连接蛋白和锚定连接蛋白更为丰富。KEGG通路分析表明，细胞色素c和IL-12A发生了显着改变。DEP与细胞信号传导，迁移，抑制，凋亡和花生四烯酸代谢的丰富有关。这些发现提高了我们对IL-35在抑制CD8 + T细胞中的作用的了解。