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Fc 伽马受体在炎症性关节炎中作为骨质破坏的调节剂。

Fc Gamma Receptors as Regulators of Bone Destruction in Inflammatory Arthritis.

机构信息

Department of Rheumatology and Immunology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Immunol. 2021 Jun 23;12:688201. doi: 10.3389/fimmu.2021.688201. eCollection 2021.

Abstract

Bone erosion is one of the primary features of inflammatory arthritis and is caused by excessive differentiation and activation of osteoclasts. Fc gamma receptors (FcγRs) have been implicated in osteoclastogenesis. Our recent studies demonstrate that joint-deposited lupus IgG inhibited RANKL-induced osteoclastogenesis. FcγRI is required for RANKL-induced osteoclastogenesis and lupus IgG-induced signaling transduction. We reviewed the results of studies that analyzed the association between FcγRs and bone erosion in inflammatory arthritis. The analysis revealed the dual roles of FcγRs in bone destruction in inflammatory arthritis. Thus, IgG/FcγR signaling molecules may serve as potential therapeutic targets against bone erosion.

摘要

骨侵蚀是炎症性关节炎的主要特征之一,是由破骨细胞过度分化和激活引起的。Fcγ 受体(FcγRs)被认为与破骨细胞生成有关。我们最近的研究表明,关节沉积的狼疮 IgG 抑制了 RANKL 诱导的破骨细胞生成。FcγRI 是 RANKL 诱导的破骨细胞生成和狼疮 IgG 诱导的信号转导所必需的。我们回顾了分析 FcγRs 与炎症性关节炎骨侵蚀之间关系的研究结果。分析结果揭示了 FcγRs 在炎症性关节炎骨破坏中的双重作用。因此,IgG/FcγR 信号分子可能成为针对骨侵蚀的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2bf2/8262610/fa7fdd4c1b2d/fimmu-12-688201-g001.jpg

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