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Ablation of the Ccr2 gene exacerbates polyarthritis in interleukin-1 receptor antagonist-deficient mice
https://doi.org/10.24517/00027537
https://doi.org/10.24517/0002753719d13a4d-912c-4ec1-b6a6-e468012e7e69
| 名前 / ファイル | ライセンス | アクション |
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ME-PR-MUKAIDA-N-96.pdf (851.4 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||||||||
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| 公開日 | 2017-10-05 | |||||||||||||||||
| タイトル | ||||||||||||||||||
| タイトル | Ablation of the Ccr2 gene exacerbates polyarthritis in interleukin-1 receptor antagonist-deficient mice | |||||||||||||||||
| 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 | |||||||||||||||||
| ID登録 | ||||||||||||||||||
| ID登録 | 10.24517/00027537 | |||||||||||||||||
| ID登録タイプ | JaLC | |||||||||||||||||
| 著者 |
Fujii, Hiroshi
× Fujii, Hiroshi× Baba, Tomohisa× Ishida, Yuko× Kondo, Toshikazu× Yamagishi, Masakazu× Kawano, Mitsuhiro× Mukaida, Naofumi |
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| 著者別表示 |
藤井, 博
× 藤井, 博
× 馬場, 智久
× 近藤, 稔和
× 山岸, 正和
× 川野, 充弘
× 向田, 直史
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| 提供者所属 | ||||||||||||||||||
| 内容記述タイプ | Other | |||||||||||||||||
| 内容記述 | 金沢大学がん研究所 | |||||||||||||||||
| 書誌情報 |
Arthritis and Rheumatism 巻 63, 号 1, p. 96-106, 発行日 2011-01-01 |
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| ISSN | ||||||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||||||
| 収録物識別子 | 0004-3591 | |||||||||||||||||
| NCID | ||||||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||||||
| 収録物識別子 | AA00551881 | |||||||||||||||||
| DOI | ||||||||||||||||||
| 関連タイプ | isVersionOf | |||||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||||
| 関連識別子 | 10.1002/art.30106 | |||||||||||||||||
| 出版者 | ||||||||||||||||||
| 出版者 | Wiley-Blackwell / the American College of Rheumatology | |||||||||||||||||
| 抄録 | ||||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||||
| 内容記述 | Objective The pathogenesis of rheumatoid arthritis (RA) involves cytokines and chemokines. Given the role of intraarticular macrophage infiltration in RA, this study was undertaken to address the pathogenic role of CCR2, a chemokine receptor that is abundantly expressed by macrophages, in Il1rn-deficient mice, a mouse model of RA. Methods Il1rn-deficient and Il1rn and Ccr2-double-deficient mice were subjected to clinical assessment of arthritis and histologic examination. Bone mineral density was measured with computed tomography. The types of cells infiltrating joints were determined by immunohistochemical analysis and flow cytometric analysis. Osteoclasts in joints were quantified after tartrate-resistant acid phosphatase staining. Cytokine and chemokine levels were measured by enzyme-linked immunosorbent assay and multiplex suspension array assay. The expression patterns of chemokines and osteoclastogenic factors were determined by double-color immunofluorescence analysis. Anti-mouse CXCR2 antibody was injected into Il1rn and Ccr2-double-deficient mice for blocking experiments. Results Ablation of the Ccr2 gene actually exacerbated arthritis and intraarticular osteoclastogenesis, while it enhanced intraarticular neutrophil but not macrophage accumulation in Il1rn-deficient mice. Infiltrated neutrophils expressed the osteoclastogenic factors RANKL and ADAM-8, thereby augmenting intraarticular osteoclastogenesis in Il1rn and Ccr2-double-deficient mice. Moreover, the double-deficient mice exhibited enhanced expression of the neutrophilic chemokines keratinocyte chemoattractant and macrophage inflammatory protein 2 (MIP-2), compared with Il1rn-deficient mice. Finally, neutralizing antibodies to CXCR2, the receptor for keratinocyte chemoattractant and MIP-2, dramatically attenuated arthritis in Il1rn and Ccr2-double-deficient mice. Conclusion Our findings indicate that CCR2-mediated signals can modulate arthritis in Il1rn-deficient mice by negatively regulating neutrophil infiltration. © 2011 by the American College of Rheumatology. | |||||||||||||||||
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| 出版タイプ | AM | |||||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||||||||||
