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肿瘤坏死因子抑制剂治疗对类风湿关节炎破骨细胞前体的影响。

Effect of Tumor Necrosis Factor Inhibitor Therapy on Osteoclasts Precursors in Rheumatoid Arthritis.

作者信息

Perpétuo Inês P, Caetano-Lopes Joana, Rodrigues Ana Maria, Campanilho-Marques Raquel, Ponte Cristina, Canhão Helena, Ainola Mari, Fonseca João E

机构信息

Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal.

Rheumatology Research Unit, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, Lisboa, Portugal; Rheumatology Department, Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, EPE, Lisbon Academic Medical Centre, Lisboa, Portugal.

出版信息

Biomed Res Int. 2017;2017:2690402. doi: 10.1155/2017/2690402. Epub 2017 Feb 13.

DOI:10.1155/2017/2690402
PMID:28286757
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5327780/
Abstract

. Tumor necrosis factor (TNF) increases circulating osteoclast (OC) precursors numbers by promoting their proliferation and differentiation. The aim of this study was to assess the effect of TNF inhibitors (TNFi) on the differentiation and activity of OC in rheumatoid arthritis (RA) patients. Seventeen RA patients treated with TNFi were analyzed at baseline and after a minimum follow-up period of 6 months. Blood samples were collected to assess receptor activator of nuclear factor kappa-B ligand (RANKL) surface expression on circulating leukocytes and frequency and phenotype of monocyte subpopulations. Quantification of serum levels of bone turnover markers, in vitro OC differentiation assays, and qRT-PCR for OC specific genes was performed. . After TNFi therapy, patients had reduced RANKL surface expression in B-lymphocytes and the frequency of circulating classical CD14CD16 monocytes was decreased. Serum levels of sRANKL, sRANKL/OPG ratio, and CTX-I were reduced in RA patients after TNFi treatment. Moreover, after exposure to TNFi, osteoclast differentiation and activity were decreased, as well as the expression of TRAF6 and cathepsin K. . We propose that TNFi arrests bone loss and erosion, through two pathways: direct reduction of osteoclast precursor numbers and inhibition of intracellular signaling pathways acting through TRAF6.

摘要

肿瘤坏死因子（TNF）通过促进破骨细胞（OC）前体细胞的增殖和分化来增加其循环数量。本研究的目的是评估TNF抑制剂（TNFi）对类风湿关节炎（RA）患者OC分化和活性的影响。对17例接受TNFi治疗的RA患者在基线时以及至少随访6个月后进行分析。采集血样以评估循环白细胞上核因子κB受体激活剂配体（RANKL）的表面表达以及单核细胞亚群的频率和表型。进行骨转换标志物血清水平的定量、体外OC分化测定以及OC特异性基因的qRT-PCR。TNFi治疗后，患者B淋巴细胞中RANKL表面表达降低，循环经典CD14CD16单核细胞的频率降低。TNFi治疗后RA患者血清sRANKL水平、sRANKL/OPG比值和I型胶原交联C末端肽（CTX-I）降低。此外，暴露于TNFi后，破骨细胞分化和活性降低，肿瘤坏死因子受体相关因子6（TRAF6）和组织蛋白酶K的表达也降低。我们提出，TNFi通过两条途径阻止骨质流失和骨侵蚀：直接减少破骨细胞前体细胞数量以及抑制通过TRAF6起作用的细胞内信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b50f/5327780/dbb1ae291ca4/BMRI2017-2690402.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b50f/5327780/204b1094fbdc/BMRI2017-2690402.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b50f/5327780/dbb1ae291ca4/BMRI2017-2690402.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b50f/5327780/204b1094fbdc/BMRI2017-2690402.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b50f/5327780/dbb1ae291ca4/BMRI2017-2690402.002.jpg

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