狼疮IgG诱导滑膜炎症但抑制SLE关节炎的骨侵蚀

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引用次数: 2

摘要

骨侵蚀是炎症性关节炎的一个重要特征。目前尚不清楚狼疮关节炎缺乏骨质侵蚀和破坏的原因。我们最近发表的论文提出了一个有趣的发现,关节沉积狼疮IgG触发滑膜炎,但抑制破骨细胞生成,负责骨破坏。本研究数据显示,关节沉积狼疮IgG通过FcgRI对单核/巨噬细胞诱导滑膜炎,并通过竞争FcgRI与RANKL结合,阻断RANKL诱导的破骨细胞生成。本研究促进了对狼疮关节炎发病机制的理解,并为抑制炎性关节炎骨破坏提供了新的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lupus IgG Induces Synovial Inflammation but Inhibits Bone Erosions in SLE Arthritis
Bone erosion is an important feature of inflammatory arthritis. It remains unknown why lupus arthritis lacks bone erosion and destruction. Our recent published paper presents the interesting discovery that joint deposited lupus IgG triggers synovitis but suppresses osteoclastogenesis which is responsible for bone destruction. In this paper, data show that joint deposited lupus IgG induces synovitis through FcgRI on monocytes/macrophages and blocks RANKL-induced osteoclastogenesis through competing for FcgRI binding with RANKL. This study promotes understanding the pathogenesis of lupus arthritis and provides a novel therapeutic target of FcgRI to inhibit bone destruction in inflammatory arthritis.
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