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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >FoxP3~+ regulatory T cells essentially contribute to peripheral CD8~+ T-cell tolerance induced by steady-state dendritic cells
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FoxP3~+ regulatory T cells essentially contribute to peripheral CD8~+ T-cell tolerance induced by steady-state dendritic cells

机译：FoxP3〜+调节性T细胞在本质上促进稳态树突状细胞诱导的外周CD8〜+ T细胞耐受性

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摘要

Peripheral T-cell tolerance is thought to significantly contribute to the prevention of autoimmunity, and it has been shown that antigen-presenting steady-state dendritic cells efficiently induce peripheral tolerance. We previously showed that dendritic-cell-induced tolerance is a T-cell-intrinsic process that depends on coinhibitory molecules such as programmed death-1. Here we specifically analyze the involvement of FoxP3~+ regulatory T cells, which are known to be important for maintenance of self-tolerance. We show that antigen presentation by steady-state dendritic cells failed to induce peripheral tolerance in the absence of FoxP3~+ regulatory T cells but induced protective CD8~+ T-cell-mediated immunity instead. Regulatory T-cell-depleted mice had massively increased numbers of dendritic cells in lymph nodes. Dendritic cells isolated from mice without regulatory T cells had up-regulated costimulatory molecules and showed stronger T-cell stimulatory capacity ex vivo, suggesting that regulatory T cells contribute to peripheral tolerance by keeping the dendritic cells in an immature state. Using blocking antibodies, we demonstrate that CTLA-4 but not IL-10 is necessary for control of dendritic cells by regulatory T cells.
机译：认为外周T细胞耐受性显着有助于自身免疫的预防，并且已经表明，呈递抗原的稳态树突状细胞有效诱导外周耐受性。我们以前表明树突状细胞诱导的耐受性是T细胞内在过程，其依赖于共抑制性分子，例如程序性死亡-1。在这里，我们专门分析FoxP3〜+调节性T细胞的参与，这对维持自我耐受很重要。我们表明，在没有FoxP3〜+调节性T细胞的情况下，稳态树突状细胞的抗原呈递未能诱导外周耐受，但诱导了保护性CD8〜+ T细胞介导的免疫。调节性T细胞缺失的小鼠淋巴结中树突状细胞数量大量增加。从没有调节性T细胞的小鼠中分离出的树突状细胞具有上调的共刺激分子，并且离体显示出更强的T细胞刺激能力，这表明调节性T细胞通过使树突状细胞保持未成熟状态而有助于外周耐受。使用封闭抗体，我们证明CTLA-4而非IL-10对于通过调节性T细胞控制树突状细胞是必需的。

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    Anita Schildknecht; Sabine Brauer; Corinne Brenner; Katharina Lahl; Hansjoerg Schild; Tim Sparwasser; Hans Christian Probst; Maries van den Broek;

  • 作者单位

    Institute of Experimental Immunology, University Hospital Zurich, 8091 Zurich, Switzerland Ontario Cancer Institute and Department of Medical Biophysics and Immunology, University of Toronto, Toronto, Ontario M5G 2C1, Canada;

    Institute for Immunology, University Medical Center Mainz, 55131 Mainz, Germany;

    Institute of Experimental Immunology, University Hospital Zurich, 8091 Zurich, Switzerland;

    Institut fur Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universitaet Muenchen, 81675 Munich, Germany;

    Institute for Immunology, University Medical Center Mainz, 55131 Mainz, Germany;

    Institut fur Medizinische Mikrobiologie, Immunologie und Hygiene, Technische Universitaet Muenchen, 81675 Munich, Germany Institute of Infection immunology,Centre for Experimental and Clinical Infection Research, Twincore, Feodor-Lynen-Strasse 7, 30625 Hannover, Germany;

    Institute for Immunology, University Medical Center Mainz, 55131 Mainz, Germany;

    Institute of Experimental Immunology, University Hospital Zurich, 8091 Zurich, Switzerland Department of Oncology, Laboratory of Tumor Immunology, University Hospital Zurich, Frauenklinikstrasse 10, 8091 Zurich, Switzerland;

  • 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);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    treg; tolerance; DC; CD8~+ T cells;

    机译：reg公差;DC;CD8〜+ T细胞;

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