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首页> 外文期刊>Allergology international: official journal of the Japanese Society of Allergology >Thrombomodulin modulates dendritic cells via both antagonism of high mobility group protein B1 and an independent mechanism
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Thrombomodulin modulates dendritic cells via both antagonism of high mobility group protein B1 and an independent mechanism

机译：血栓调节蛋白通过高迁移率族蛋白B1的拮抗作用和独立机制调节树突状细胞

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Background: Thrombomodulin treatment modulates the properties of dendritic cells (DCs) converting them from immunogenic to tolerogenic and inducing its own expression on DCs. Thrombomodulin binds to the inflammatory mediator, high mobility group protein B1 (HMGB1), antagonizing signalling through its receptor, receptor for advanced glycation end products (RAGE). Methods: To test if soluble thrombomodulin could antagonize HMGB1 signaling via RAGE on DCs. DCs were prepared from mouse bone marrow cells or human monocytes. In some experiments dendritic cells were sorted into thrombomodulin+ and thrombomodulin- populations. Expression of surface maturation markers was determined by flow cytometry following treatment with thrombomodulin in the presence or absence of HMGB1. Results: Thrombomodulin+ dendritic cells secrete less HMGB1 into the medium. HMGB1 reduces the effects of thrombomodulin on expression of DC maturation markers. Treatment with thrombomodulin reduces the expression of maturation markers such as CD80 and CD86 and increases the expression of thrombomodulin on the DC surface. Treatment of DCs with neutralizing anti-HMGB1 antibody acted synergistically with thrombomodulin in increasing thrombomodulin expression on DCs. Treatment with thrombomodulin can still reduce the expression of surface markers on DCs derived from mice that are deficient in RAGE showing that thrombomodulin can affect DCs by an alternative mechanism. Conclusions: The results of this study show that thrombomodulin modulates DCs both by antagonizing the interaction of HMGB1 with RAGE and by an independent mechanism.
机译：背景：血栓调节素治疗可调节树突状细胞（DC）的特性，将其从免疫原性转变为耐受性，并诱导其在DC上的表达。血栓调节蛋白与炎性介质高迁移率族蛋白B1（HMGB1）结合，通过其受体（高级糖基化终产物（RAGE）的受体）拮抗信号传导。方法：测试可溶性血栓调节蛋白是否可通过DC上的RAGE拮抗HMGB1信号。从小鼠骨髓细胞或人单核细胞制备DC。在一些实验中，将树突状细胞分类为血栓调节蛋白+和血栓调节蛋白-群体。在存在或不存在HMGB1的情况下，用血栓调节蛋白治疗后，通过流式细胞术确定表面成熟标志物的表达。结果：血栓调节蛋白+树突状细胞向培养基中分泌的HMGB1较少。 HMGB1减少血栓调节蛋白对DC成熟标志物表达的影响。血栓调节蛋白的治疗降低了成熟标记物（例如CD80和CD86）的表达，并增加了血栓调节蛋白在DC表面的表达。用中和性抗HMGB1抗体治疗DC与血栓调节素协同作用，增加DC上的血栓调节素表达。用血栓调节蛋白治疗仍可降低源自RAGE缺陷型小鼠的DC上表面标志物的表达，这表明血栓调节蛋白可通过其他机制影响DC。结论：这项研究的结果表明，血栓调节蛋白通过拮抗HMGB1与RAGE的相互作用以及独立机制来调节DC。

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