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CTRP6 is an endogenous complement regulator that can effectively treat induced arthritis
http://hdl.handle.net/10069/35994
http://hdl.handle.net/10069/3599499301ca2-d6cc-42c1-b34a-b61e42a9e204
名前 / ファイル | ライセンス | アクション |
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NaCom6_8483.pdf (2.3 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2015-11-30 | |||||
タイトル | ||||||
タイトル | CTRP6 is an endogenous complement regulator that can effectively treat induced arthritis | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Murayama, Masanori A.
× Murayama, Masanori A.× Kakuta, Shigeru× Inoue, Asuka× Umeda, Naoto× Yonezawa, Tomo× Maruhashi, Takumi× Tateishi, Koichiro× Ishigame, Harumichi× Yabe, Rikio× Ikeda, Satoshi× Seno, Akimasa× Chi, Hsi-Hua× Hashiguchi, Yuriko× Kurata, Riho× Tada, Takuya× Kubo, Sachiko× Sato, Nozomi× Liu, Yang× Hattori, Masahira× Saijo, Shinobu× Matsushita, Misao× Fujita, Teizo× Sumida, Takayuki× Iwakura, Yoichiro |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | The complement system is important for the host defence against infection as well as for the development of inflammatory diseases. Here we show that C1q/TNF-related protein 6 (CTRP6; gene symbol C1qtnf6) expression is elevated in mouse rheumatoid arthritis (RA) models. C1qtnf6 -/- mice are highly susceptible to induced arthritis due to enhanced complement activation, whereas C1qtnf6-transgenic mice are refractory. The Arthus reaction and the development of experimental autoimmune encephalomyelitis are also enhanced in C1qtnf6 -/- mice and C1qtnf6 -/- embryos are semi-lethal. We find that CTRP6 specifically suppresses the alternative pathway of the complement system by competing with factor B for C3(H 2 O) binding. Furthermore, treatment of arthritis-induced mice with intra-articular injection of recombinant human CTRP6 cures the arthritis. CTRP6 is expressed in human synoviocytes, and CTRP6 levels are increased in RA patients. These results indicate that CTRP6 is an endogenous complement regulator and could be used for the treatment of complement-mediated diseases. | |||||
書誌情報 |
Nature Communications 巻 6, p. 8483, 発行日 2015-09-25 |
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出版者 | ||||||
出版者 | Nature Publishing Group | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 20411723 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1038/ncomms9483 | |||||
権利 | ||||||
権利情報 | This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Nature Communications, 6, 8483; 2015 |