Changes in the T cell surface redox environment regulate critical cell functions, such as cell migration, viral entry and cytokine production. Cell surface protein disulfide isomerase (PDI) contributes to the regulation of T cell surface redox status. Cell surface PDI can be released into the extracellular milieu or can be internalized by T cells. We have found that galectin-9, a soluble lectin expressed by T cells, endothelial cells and dendritic cells, binds to and retains PDI on the cell surface. While endogenous galectin-9 is not required for basal cell surface PDI expression, exogenous galectin-9 mediated retention of cell surface PDI shifted the disulfide/thiol equilibrium on the T cell surface. O-glycans on PDI are required for galectin-9 binding, and PDI recognition appears to be specific for galectin-9, as galectin-1 and galectin-3 do not bind PDI. Galectin-9 is widely expressed by immune and endothelial cells in inflamed tissues, suggesting that T cells would be exposed to abundant galectin-9, in cis and in trans, in infectious or autoimmune conditions.

中文翻译：

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Galectin-9与蛋白质二硫键异构酶上的O-聚糖结合

T细胞表面氧化还原环境的变化调节了关键的细胞功能，例如细胞迁移，病毒进入和细胞因子的产生。细胞表面蛋白二硫键异构酶（PDI）有助于调节T细胞表面氧化还原状态。细胞表面PDI可以释放到细胞外环境中，也可以被T细胞内在化。我们已经发现，galectin-9（一种由T细胞，内皮细胞和树突状细胞表达的可溶性凝集素）与PDI结合并保留在细胞表面。虽然基础细胞表面PDI的表达不需要内源半乳糖凝集素9，但外源半乳糖凝集素9介导的细胞表面PDI保留可改变T细胞表面的二硫键/硫醇平衡。Øgalectin-9结合需要PDI上的β-聚糖，而PDI识别似乎是针对galectin-9特异的，因为galectin-1和galectin-3不结合PDI。Galectin-9在发炎组织中的免疫细胞和内皮细胞中广泛表达，这表明T细胞在传染性或自身免疫性条件下，无论是顺式还是反式，都将暴露于丰富的Galectin-9中。