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首页> 外文期刊>Nature immunology >Hobit- and Blimp-1-driven CD4(+) tissue-resident memory T cells control chronic intestinal inflammation
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Hobit- and Blimp-1-driven CD4(+) tissue-resident memory T cells control chronic intestinal inflammation

机译：呼吸博客和Blimp-1驱动CD4（+）组织 - 植物记忆记忆T细胞控制慢性肠炎

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摘要

Although tissue-resident memory T cells (T-RM cells) have been shown to regulate host protection in infectious disorders, their function in inflammatory bowel disease (IBD) remains to be investigated. Here we characterized T-RM cells in human IBD and in experimental models of intestinal inflammation. Pro-inflammatory T-RM cells accumulated in the mucosa of patients with IBD, and the presence of CD4(+)CD69(+)CD103(+) T-RM cells was predictive of the development of flares. In vivo, functional impairment of T-RM cells in mice with double knockout of the T-RM-cell-associated transcription factors Hobit and Blimp-1 attenuated disease in several models of colitis, due to impaired cross-talk between the adaptive and innate immune system. Finally, depletion of T-RM cells led to a suppression of colitis activity. Together, our data demonstrate a central role for T-RM cells in the pathogenesis of chronic intestinal inflammation and suggest that these cells could be targets for future therapeutic approaches in IBD.
机译：虽然已经显示组织 - 驻留记忆T细胞（T-RM细胞）调节传染病中的宿主保护，但它们在炎症性肠病（IBD）中的功能仍有待研究。在这里，我们在人IBD中表征了T-RM细胞以及肠道炎症的实验模型。积聚在IBD患者的粘膜中的促炎T-RM细胞，以及CD4（+）CD69（+）CD103（+）T-RM细胞的存在预测耀斑的发育。在体内，用双敲除T-RM细胞相关转录因子呼吸博客和Blimp-1减毒疾病的小鼠中T-RM细胞的功能损伤，由于自适应和先天内的串扰受损免疫系统。最后，耗尽T-RM细胞导致结肠炎活性的抑制。我们的数据在一起证明了T-RM细胞在慢性肠炎症的发病机制中的核心作用，并表明这些细胞可以是IBD中未来治疗方法的目标。

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  • 来源
    《Nature immunology》 |2019年第3期|共15页
  • 作者

    Zundler Sebastian; Becker Emily; Spocinska Marta; Slawik Monique; Parga-Vidal Loreto; Stark Regina; Wiendl Maximilian; Atreya Raja; Rath Timo; Leppkes Moritz; Hildner Kai; Lopez-Posadas Rocio; Lukassen Soeren; Ekici Arif B.; Neufert Clemens; Atreya Imke; van Gisbergen Klaas P. J. M.; Neurath Markus F.;

  • 作者单位

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Univ Amsterdam Amsterdam UMC Sanquin Res &

    Landsteiner Lab Dept Hematopoiesis Amsterdam;

    Univ Amsterdam Amsterdam UMC Sanquin Res &

    Landsteiner Lab Dept Hematopoiesis Amsterdam;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Inst Human Genet Erlangen Germany;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Inst Human Genet Erlangen Germany;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

    Univ Amsterdam Amsterdam UMC Sanquin Res &

    Landsteiner Lab Dept Hematopoiesis Amsterdam;

    Friedrich Alexander Univ FAU Erlangen Nurnberg Kussmaul Campus Med Res &

    Translat Res Ctr Dept;

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  • 正文语种 eng
  • 中图分类 医学免疫学;
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