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首页> 外文期刊>Infection and immunity >Involvement of SOCS3 in Regulation of CD11c+ Dendritic Cell-Derived Osteoclastogenesis and Severe Alveolar Bone Loss
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Involvement of SOCS3 in Regulation of CD11c+ Dendritic Cell-Derived Osteoclastogenesis and Severe Alveolar Bone Loss

机译：SOCS3参与调节CD11c +树突状细胞衍生的破骨细胞生成和严重的肺泡骨丢失

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To investigate the role of suppressor of cytokine signaling (SOCS) molecules in periodontal immunity and RANKL-mediated dendritic cell (DC)-associated osteoclastogenesis, we analyzed SOCS expression profiles in CD4+ T cells and the effect of SOCS3 expression in CD11c+ DCs during periodontal inflammation-induced osteoclastogenesis and bone loss in nonobese diabetic (NOD) versus humanized NOD/SCID mice. Our results of ex vivo and in vitro analyses showed that (i) there is significantly higher SOCS3 expression associated with RANKL+ T-cell-mediated bone loss in correlation with increased CD11c+ DC-mediated osteoclastogenesis; (ii) the transfection of CD11c+ DC using an adenoviral vector carrying a dominant negative SOCS3 gene significantly abrogates TRAP and bone-resorptive activity; and (iii) inflammation-induced TRAP expression, bone resorption, and SOCS3 activity are not associated with any detectable change in the expression levels of TRAF6 and mitogen-activated protein kinase signaling adaptors (i.e., Erk, Jnk, p38, and Akt) in RANKL+ T cells. We conclude that SOCS3 plays a critical role in modulating cytokine signaling involved in RANKL-mediated DC-derived osteoclastogenesis during immune interactions with T cells and diabetes-associated severe inflammation-induced alveolar bone loss. Therefore, the development of SOCS3 inhibitors may have therapeutic potential as the target to halt inflammation-induced bone loss under pathological conditions in vivo.
机译：为了研究细胞因子信号抑制因子（SOCS）在牙周免疫和RANKL介导的树突状细胞（DC）相关破骨细胞形成中的作用，我们分析了CD4 + T细胞中SOCS的表达概况以及与非人源化NOD / SCID小鼠相比，非肥胖糖尿病（NOD）牙周炎症诱导的破骨细胞生成和骨丢失期间CD11c + DC中的SOCS3表达。我们的离体和体外分析结果表明：（i）与RANKL + T细胞介导的骨丢失相关的SOCS3表达显着高于CD11c + DC介导的破骨细胞生成; （ii）使用带有显性负SOCS3基因的腺病毒载体转染CD11c + DC可显着消除TRAP和骨吸收活性。 （iii）炎症诱导的TRAP表达，骨吸收和SOCS3活性与TRAF6和丝裂原激活的蛋白激酶信号转导子（即Erk，Jnk，p38和Akt）的表达水平的任何可检测变化无关。 RANKL + T细胞。我们得出结论，SOCS3在调节与T细胞和糖尿病相关的严重炎症诱导的牙槽骨丢失的免疫相互作用过程中参与RANKL介导的DC衍生的破骨细胞发生的细胞因子信号传导中起关键作用。因此，SOCS3抑制剂的开发可能具有治疗潜力，作为在体内病理条件下制止炎症引起的骨丢失的靶标。

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