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自身抗体 IgG 对破骨细胞生成的调控作用。

Regulatory effects of autoantibody IgG on osteoclastogenesis.

机构信息

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

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

出版信息

Clin Immunol. 2023 Jan;246:109200. doi: 10.1016/j.clim.2022.109200. Epub 2022 Nov 23.

DOI:10.1016/j.clim.2022.109200
PMID:36435446
Abstract

Inflammatory arthritis is common in both systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and eventually leads to bone homeostasis disorders. However, RA patients generally have severe bone destruction, which is rare in SLE patients. Recent studies have demonstrated that anti-citrullinated protein antibodies are important factors leading to bone destruction in RA. On the other hand, SLE patients present deposition of autoantibodies in the joints, which plays an important role in bone protection. These different phenomena occur because of the effects of the autoantibodies on the monocytes/macrophages during osteoclastogenesis, and the mechanisms underlying these effects differ between SLE and RA patients.

摘要

炎症性关节炎在系统性红斑狼疮 (SLE) 和类风湿关节炎 (RA) 中都很常见,并最终导致骨稳态紊乱。然而,RA 患者通常会出现严重的骨质破坏,而 SLE 患者则很少见。最近的研究表明,抗瓜氨酸化蛋白抗体是导致 RA 骨质破坏的重要因素。另一方面,SLE 患者的关节中会沉积自身抗体,这对骨保护起着重要作用。这些不同的现象是由于自身抗体在破骨细胞形成过程中对单核细胞/巨噬细胞的影响所致,而 SLE 和 RA 患者的这些影响机制不同。

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引用本文的文献

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IgG promotes TNF-α induced osteoclastogenesis by upregulating the expression of TNFR1 and the NF-κB signalling pathway.免疫球蛋白G通过上调肿瘤坏死因子受体1的表达和核因子κB信号通路促进肿瘤坏死因子-α诱导的破骨细胞生成。
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2
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