The molecular mechanism of osteoclastogenesis in rheumatoid arthritis.

Arthritis Research Pub Date : 2002-01-01 Epub Date: 2002-04-12 DOI:10.1186/ar431
Nobuyuki Udagawa, Shigeru Kotake, Naoyuki Kamatani, Naoyuki Takahashi, Tatsuo Suda
{"title":"The molecular mechanism of osteoclastogenesis in rheumatoid arthritis.","authors":"Nobuyuki Udagawa,&nbsp;Shigeru Kotake,&nbsp;Naoyuki Kamatani,&nbsp;Naoyuki Takahashi,&nbsp;Tatsuo Suda","doi":"10.1186/ar431","DOIUrl":null,"url":null,"abstract":"<p><p>Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte-macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-kappaB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Recent studies have shown that T lymphocytes produce cytokines other than RANKL such as IL-17, granulocyte-macrophage colony-stimulating factor and IFN-gamma, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.</p>","PeriodicalId":8403,"journal":{"name":"Arthritis Research","volume":"4 5","pages":"281-9"},"PeriodicalIF":0.0000,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/ar431","citationCount":"129","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Arthritis Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1186/ar431","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2002/4/12 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 129

Abstract

Bone-resorbing osteoclasts are formed from hemopoietic cells of the monocyte-macrophage lineage under the control of bone-forming osteoblasts. We have cloned an osteoblast-derived factor essential for osteoclastogenesis, the receptor activator of NF-kappaB ligand (RANKL). Synovial fibroblasts and activated T lymphocytes from patients with rheumatoid arthritis also express RANKL, which appears to trigger bone destruction in rheumatoid arthritis as well. Recent studies have shown that T lymphocytes produce cytokines other than RANKL such as IL-17, granulocyte-macrophage colony-stimulating factor and IFN-gamma, which have powerful regulatory effects on osteoclastogenesis. The possible roles of RANKL and other cytokines produced by T lymphocytes in bone destruction are described.

Abstract Image

Abstract Image

Abstract Image

类风湿关节炎中破骨细胞发生的分子机制。
骨吸收破骨细胞是在成骨细胞的控制下由单核-巨噬细胞谱系的造血细胞形成的。我们克隆了一种成骨细胞衍生的破骨细胞生成所必需的因子,nf - κ b配体受体激活因子(RANKL)。类风湿性关节炎患者的滑膜成纤维细胞和活化的T淋巴细胞也表达RANKL,这似乎也会引发类风湿性关节炎的骨破坏。最近的研究表明,T淋巴细胞产生除RANKL外的细胞因子,如IL-17、粒细胞-巨噬细胞集落刺激因子和ifn - γ等,对破骨细胞的发生具有强大的调节作用。描述了RANKL和T淋巴细胞产生的其他细胞因子在骨破坏中的可能作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信