|
フルヤ タケフミ
Furuya Takefumi
古谷 武文 所属 医学部 医学科（東京女子医科大学病院） 職種 非常勤講師 |
|
| 論文種別 | 原著 |
| 言語種別 | 英語 |
| 査読の有無 | 査読あり |
| 表題 | IL-23 induces human osteoclastogenesis via IL-17 in vitro, and anti-IL-23 antibody attenuates collagen-induced arthritis in rats. |
| 掲載誌名 | 正式名：Arthritis research & therapy 略 称：Arthritis Res Ther ISSNコード：(1478-6362)1478-6354(Linking) |
| 掲載区分 | 国外 |
| 巻・号・頁 | 9(5),pp.R96 |
| 著者・共著者 | Yago Toru, Nanke Yuki, Kawamoto Manabu, Furuya Takefumi, Kobashigawa Tsuyoshi, Kamatani Naoyuki, Kotake Shigeru |
| 発行年月 | 2007 |
| 概要 | This study demonstrates that IL-23 stimulates the differentiation of human osteoclasts from peripheral blood mononuclear cells (PBMC). Furthermore, in vivo blockade of endogenous IL-23 activity by treatment with anti-IL-23 antibody attenuates collagen-induced arthritis in rats by preventing both inflammation and bone destruction. IL-23 induced human osteoclastogenesis in cultures of PBMC in the absence of osteoblasts or exogenous soluble-receptor activator of NF-kappaB ligand (RANKL). This IL-23-induced osteoclastogenesis was inhibited by osteoprotegerin, anti-IL-17 antibody, and etanercept, suggesting that RANKL, IL-17, and TNF-alpha are involved. In addition, we found the ratio of production levels of IL-17 to those of IFN-gamma from activated human T cells was elevated at 1 to 10 ng/ml IL-23. The inductive effect of IL-17 and the inhibitory effect of IFN-gamma on osteoclastogenesis indicate that the balance of these two cytokines is particularly important. We also demonstrated that IL-23 administered at a later stage significantly reduced paw volume in rats with collagen-induced arthritis, in a dose-dependent manner. Furthermore, anti-IL-23 antibody reduced synovial tissue inflammation and bone destruction in these rats. These findings suggest that IL-23 is important in human osteoclastogenesis and that neutralizing IL-23 after onset of collagen-induced arthritis has therapeutic potential. Thus, controlling IL-23 production and function could be a strategy for preventing inflammation and bone destruction in patients with rheumatoid arthritis. |
| DOI | 10.1186/ar2297 |
| PMID | 17888176 |