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[原著]Type II interleukin-4 receptor-mediated anti-inflammatory response in Mm1 and J774.1 macrophages
http://hdl.handle.net/20.500.12000/0002017765
http://hdl.handle.net/20.500.12000/0002017765cc51dad7-8956-4573-8073-f90509b2ef47
名前 / ファイル | ライセンス | アクション |
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v3234p69.pdf
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Item type | デフォルトアイテムタイプ(フル)(1) | |||||||||
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公開日 | 2015-04-24 | |||||||||
タイトル | ||||||||||
タイトル | [原著]Type II interleukin-4 receptor-mediated anti-inflammatory response in Mm1 and J774.1 macrophages | |||||||||
言語 | ja | |||||||||
作成者 |
Lin, Yanhui
× Lin, Yanhui
× Kato, Seiya
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アクセス権 | ||||||||||
アクセス権 | open access | |||||||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||||||
権利情報 | ||||||||||
言語 | ja | |||||||||
権利情報 | 琉球医学会 | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | IL-4 | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | IL-13 | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | receptor | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | macrophage | |||||||||
主題 | ||||||||||
言語 | en | |||||||||
主題Scheme | Other | |||||||||
主題 | inflammation | |||||||||
内容記述 | ||||||||||
内容記述タイプ | Other | |||||||||
内容記述 | Introduction: Macrophages are involved in various inflammatory processes. Although the therapeutic potential of interleukin-4 (IL-4)-mediated immunomodulation has been proposed, it has not yet been established. The type I IL-4 receptor (IL-4RI) consists of IL-4R α and a common γ chain, whereas the type II IL-4R (IL-4RII) is a heterodimer of IL-4R a and IL-13R α 1. In the present study, we assessed the selective activation of IL-4R isoforms in the mouse macrophage cell lines, Mm1 and J774.1, to investigate the role of receptor-specific signaling in inflammatory activation. Materials and Methods: The plasmid expressing murine IL-4/ Q116E, which is analogous to the human IL-4RI-specific agonist IL-4/ R121E, was transfected to assess IL-4RI activation. IL-4RII activation was induced by IL-13. Activation of IL-4R isoforms was confirmed by the activation of signal transducer and activator of transcription 6 (STAT6). Lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) induction was examined using real-time polymerase chain reaction. LPS plus interferon- γ (INF- γ )-stimulated inducible nitric oxide synthase induction was tested using western blotting. Results: IL-4/ Q116E induced STAT6 activation in Mm1 cells but not in J774.1 cells. In Mm1 cells, IL-4/ Q116E-induced STAT6 activation was inhibited by kaempferol, a specific inhibitor for Janus kinase 3 (JAK3). IL-4/Q116E did not exhibit anti-inflammatory activity in either macrophage cell line. However, IL-13 inhibited inflammatory activation of these cells. Conclusions: Our data suggest that Mm1 cells expressed both IL-4RI and IL-4RII, whereas J774.1 cells expressed only IL-4RII. Although IL-4R isoform expression pattern was diverse in these two macrophages, the IL-4-mediated antiinflammatory effect was thought to be largely dependent on IL-4RII-mediated signaling. Thus, we could further conclude that IL-4 signaling plays a pivotal role in the regulation of macrophage inflammatory proprieties. Understanding IL-4-mediated anti-inflammatory signaling in macrophages may be beneficial for the development of therapeutics. | |||||||||
内容記述 | ||||||||||
内容記述タイプ | Other | |||||||||
内容記述 | 論文 | |||||||||
出版者 | ||||||||||
出版者 | 琉球医学会 | |||||||||
言語 | ja | |||||||||
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 | |||||||||
出版タイプ | ||||||||||
出版タイプ | VoR | |||||||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||||||
収録物識別子 | ||||||||||
収録物識別子タイプ | ISSN | |||||||||
収録物識別子 | 1346-888X | |||||||||
収録物識別子 | ||||||||||
収録物識別子タイプ | NCID | |||||||||
収録物識別子 | AN10369445 | |||||||||
収録物名 | ||||||||||
収録物名 | 琉球医学会誌 = Ryukyu Medical Journal | |||||||||
言語 | ja | |||||||||
書誌情報 |
巻 32, 号 3・4, p. 69-78 |