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首页> 外文期刊>Journal of Cellular Physiology >Intravenous Immunoglobulin (IVIG) Attenuates TNF-Induced Pathologic Bone Resorption and Suppresses Osteoclastogenesis by Inducing A20 Expression
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Intravenous Immunoglobulin (IVIG) Attenuates TNF-Induced Pathologic Bone Resorption and Suppresses Osteoclastogenesis by Inducing A20 Expression

机译：静脉注射免疫球蛋白(丙种球蛋白)变弱TNF-Induced病理骨吸收通过诱导表达A20抑制Osteoclastogenesis表达式

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Investigations on the therapeutic effects of intravenous immunoglobulin (IVIG) have focused on the suppression of autoantibody and immune complex-mediated inflammatory pathogenesis. Inflammatory diseases such as rheumatoid arthritis are often accompanied by excessive bone erosion but the effect of IVIG on osteoclasts, bone-resorbing cells, has not been studied. Here, we investigate whether IVIG directly regulates osteoclast differentiation and has therapeutic potential for suppressing osteoclast-mediated pathologic bone resorption. IVIG or cross-linking of Fc receptors with plate-bound IgG suppressed receptor activator of nuclear factor- B ligand (RANKL)-induced osteoclastogenesis and expression of osteoclast-related genes such as integrin 3 and cathepsin K in a dose-dependent manner. Mechanistically, IVIG or plate-bound IgG suppressed osteoclastogenesis by downregulating RANKL-induced expression of NFATC1, the master regulator of osteoclastogenesis. IVIG suppressed NFATC1 expression by attenuating RANKL-induced NF-B signaling, explained in part by induction of the inflammatory signaling inhibitor A20. IVIG administration attenuated in vivo osteoclastogenesis and suppressed bone resorption in the tumor necrosis factor (TNF)-induced calvarial osteolysis model. Our findings show that, in addition to suppressing inflammation, IVIG directly inhibits osteoclastogenesis through a mechanism involving suppression of RANK signaling. Direct suppression of osteoclast differentiation may provide beneficial effects on preserving bone mass when IVIG is used to treat rheumatic disorders. J. Cell. Physiol. 231: 449-458, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：调查的治疗效果静脉注射免疫球蛋白(丙种球蛋白)的关注自身抗体和免疫抑制complex-mediated炎症发病机制。炎症性疾病,如类风湿关节炎往往伴随着过度骨侵蚀但丙种球蛋白对破骨细胞的影响,微细胞,并没有被研究过。我们调查是否丙种球蛋白直接调节破骨细胞分化,并治疗抑制osteoclast-mediated潜力病理性骨吸收。plate-bound Fc受体的免疫球蛋白g抑制核因子- B配体的受体激活(RANKL)全身osteoclastogenesis和表达osteoclast-related基因整合素等3以剂量依赖性的方式和组织蛋白酶K。从力学上看,丙种球蛋白或plate-bound免疫球蛋白抑制osteoclastogenesis通过下调NFATC1 RANKL-induced表达式,主人osteoclastogenesis调节器。NFATC1表达式由衰减RANKL-inducedNF-B信号的感应部分中解释炎症信号传导抑制剂的样子。政府减毒在体内osteoclastogenesis和抑制骨吸收在全身的肿瘤坏死因子(TNF)颅顶的骨质溶解模型。,除了抑制炎症,丙种球蛋白直接抑制osteoclastogenesis通过机制包括抑制等级信号。分化可能提供有益的影响当使用丙种球蛋白治疗保留骨量风湿性疾病。449 - 458年,2016年。

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