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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB
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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

机译：耐受性和M2（替代）巨噬细胞极化是p50核因子κB调控的相关过程

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摘要

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-κB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-κB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-κB inhibits NF-KB-driven, M1-polarizing, IFN-β production. Accordingly, p50-deficient mice show exacerbated M1-driven inflammation and defective capacity to mount allergy and helminth-driven M2-polarized inflammatory reactions. Thus, NF-κB p50 is a key component in the orchestration of M2-driven inflammatory reactions.
机译：单核细胞-巨噬细胞谱系的细胞在协调和消炎中起着重要作用。可塑性是单核吞噬细胞的标志，响应环境信号，这些细胞经历不同形式的极化激活，其极端称为经典或M1以及替代或M2。 NF-κB是炎症和消融的关键调节剂，其激活受多种调节水平的控制，包括抑制作用，可以很好地调节巨噬细胞的功能。在这里，我们确定了NF-κB的p50亚基是体内外M2驱动的炎症反应的关键调节剂。 p50NF-κB抑制NF-KB驱动的M1极化IFN-β的产生。因此，p50缺陷的小鼠表现出加剧的M1驱动的炎症和缺陷的能力引起过敏和蠕虫驱动的M2极化的炎症反应。因此，NF-κBp50是编排M2驱动的炎症反应的关键成分。

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    Chiara Porta; Monica Rimoldi; Geert Raes; Lea Brys; Pietro Ghezzi; Diana Di Liberto; Francesco Dieli; Serena Ghisletti; Gioacchino Natoli; Patrick De Baetselier; Alberto Mantovani; Antonio Sica;

  • 作者单位

    Fondazione Humanitas per la Ricerca, 20089 Rozzano, Italy Dipartimento di Scienze Chimiche, Alimentari, Farmaceutiche e Farmacologiche, University of Piemonte Orientale A. Avogadro, 28100 Novara, Italy;

    Istituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico, 20089 Rozzano, Italy;

    Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, and Department of Molecular ad Cellular Interactions, 1050 Brussels, Belgium;

    Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, and Department of Molecular ad Cellular Interactions, 1050 Brussels, Belgium;

    Brighton and Sussex Medical School, Brighton BN1 9PX, United Kingdom;

    Dipartimento di Biopatologia e Metodologie Biochimediche, Universita di Palermo, 90134 Palermo, Italy;

    Dipartimento di Biopatologia e Metodologie Biochimediche, Universita di Palermo, 90134 Palermo, Italy;

    Department of Experimental Oncology, European Institute of Oncology at IFOM-IEO Campus, 20139 Milan, Italy;

    Department of Experimental Oncology, European Institute of Oncology at IFOM-IEO Campus, 20139 Milan, Italy;

    Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, and Department of Molecular ad Cellular Interactions, 1050 Brussels, Belgium;

    Istituto Clinico Humanitas, Istituto di Ricovero e Cura a Carattere Scientifico, 20089 Rozzano, Italy University of Milan, 20133 Milan, Italy;

    Fondazione Humanitas per la Ricerca, 20089 Rozzano, Italy Dipartimento di Scienze Chimiche, Alimentari, Farmaceutiche e Farmacologiche, University of Piemonte Orientale A. Avogadro, 28100 Novara, Italy;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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