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Three pentraxins C-reactive protein, serum amyloid p component and pentraxin 3 mediate complement activation using Collectin CL-P1
http://hdl.handle.net/10659/00006019
http://hdl.handle.net/10659/00006019cd01be85-ab81-417d-822a-84b4ac2d156f
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
R-2018-69_ohtani (1.4 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2019-08-08 | |||||
| タイトル | ||||||
| タイトル | Three pentraxins C-reactive protein, serum amyloid p component and pentraxin 3 mediate complement activation using Collectin CL-P1 | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Collectin | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Pentraxin | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Complement | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Classical pathway | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Alternative pathway | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | Terminal complement complex | |||||
| 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 |
Roy, Nitai
× Roy, Nitai× Ohtani, Katsuki× Hidaka, Yoshihiko× Amano, Yoshiro× Matsuda, Yasuyuki× Mori, Kenichiro× Hwang, Insu× Inoue, Norimitsu× Wakamiya, Nobutaka |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | 【Background】Pentraxins (PTXs) are a superfamily of multifunctional conserved proteins involved in acute-phase responses. Recently, we have shown that collectin placenta 1 (CL-P1) and C-reactive protein (CRP) mediated complement activation and failed to form terminal complement complex (TCC) in normal serum conditions because of complement factor H inhibition.【Methods】We used CL-P1 expressing CHO/ldlA7 cells to study the interaction with PTXs. Soluble type CL-P1 was used in an ELISA assay for the binding, C3 and TCC deposition experiments. Furthermore, we used our previously established CL-P1 expressing HEK293 cells for the C3 fragment and TCC deposition assay.【Results】We demonstrated that CL-P1 also bound serum amyloid p component (SAP) and pentraxin 3 (PTX3) to activate the classical pathway and the alternative pathway using factor B. CRP and PTX3 further amplified complement deposition by properdin. We found that CRP and PTX3 recruit CFH, whereas SAP recruits C4 binding protein on CL-P1 expressing cell surfaces to prevent the formation of TCC in normal serum conditions. In addition, depletion of CFH, C4BP and complement factor I (CFI) failed to prevent TCC formation both in ELISA and cell experiments. Furthermore, soluble complement receptor 1, an inhibitor of all complement pathways prevents PTX induced TCC formation.【Conclusion】Our current study hypothesizes that the interaction of pentraxins with CL-P1 is involved in complement activation.【General significance】CL-P1 might generally inhibit PTX induced complement activation and host damage to protect self-tissues. | |||||
| 書誌情報 |
Biochimica et Biophysica Acta (BBA) - General Subjects 巻 1861, 号 2, p. 1-14, 発行日 2017-02 |
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| ISBN | ||||||
| 識別子タイプ | ISBN | |||||
| 関連識別子 | 0006-3002 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | http://dx.doi.org/10.1016/j.bbagen.2016.11.023 | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
| 出版者 | ||||||
| 出版者 | Elsevier B.V. | |||||
| 資源タイプ | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Article | |||||
