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Rbpj expression in regulatory T cells is critical for restraining TH2 responses

Author

Listed:
  • Michael Delacher

    (University Regensburg and University Hospital Regensburg
    University Regensburg and University Hospital Regensburg
    German Cancer Research Center (DKFZ))

  • Christian Schmidl

    (University Regensburg and University Hospital Regensburg)

  • Yonatan Herzig

    (Weizmann Institute of Science)

  • Minka Breloer

    (Bernhard Nocht Institute for Tropical Medicine)

  • Wiebke Hartmann

    (Bernhard Nocht Institute for Tropical Medicine)

  • Fabian Brunk

    (German Cancer Research Center (DKFZ))

  • Danny Kägebein

    (German Cancer Research Center (DKFZ))

  • Ulrike Träger

    (German Cancer Research Center (DKFZ))

  • Ann-Cathrin Hofer

    (German Cancer Research Center (DKFZ))

  • Sebastian Bittner

    (University Regensburg and University Hospital Regensburg
    University Regensburg and University Hospital Regensburg)

  • Dieter Weichenhan

    (German Cancer Research Center (DKFZ))

  • Charles D. Imbusch

    (German Cancer Research Center (DKFZ))

  • Agnes Hotz-Wagenblatt

    (German Cancer Research Center (DKFZ))

  • Thomas Hielscher

    (German Cancer Research Center (DKFZ))

  • Achim Breiling

    (German Cancer Research Center (DKFZ))

  • Giuseppina Federico

    (German Cancer Research Center (DKFZ))

  • Hermann-Josef Gröne

    (German Cancer Research Center (DKFZ))

  • Roland M. Schmid

    (Technical University of Munich)

  • Michael Rehli

    (University Regensburg and University Hospital Regensburg
    University Hospital Regensburg)

  • Jakub Abramson

    (Weizmann Institute of Science)

  • Markus Feuerer

    (University Regensburg and University Hospital Regensburg
    University Regensburg and University Hospital Regensburg
    German Cancer Research Center (DKFZ))

Abstract

The transcriptional regulator Rbpj is involved in T-helper (TH) subset polarization, but its function in Treg cells remains unclear. Here we show that Treg-specific Rbpj deletion leads to splenomegaly and lymphadenopathy despite increased numbers of Treg cells with a polyclonal TCR repertoire. A specific defect of Rbpj-deficient Treg cells in controlling TH2 polarization and B cell responses is observed, leading to the spontaneous formation of germinal centers and a TH2-associated immunoglobulin class switch. The observed phenotype is environment-dependent and can be induced by infection with parasitic nematodes. Rbpj-deficient Treg cells adopt open chromatin landscapes and gene expression profiles reminiscent of tissue-derived TH2-polarized Treg cells, with a prevailing signature of the transcription factor Gata-3. Taken together, our study suggests that Treg cells require Rbpj to specifically restrain TH2 responses, including their own excessive TH2-like differentiation potential.

Suggested Citation

  • Michael Delacher & Christian Schmidl & Yonatan Herzig & Minka Breloer & Wiebke Hartmann & Fabian Brunk & Danny Kägebein & Ulrike Träger & Ann-Cathrin Hofer & Sebastian Bittner & Dieter Weichenhan & Ch, 2019. "Rbpj expression in regulatory T cells is critical for restraining TH2 responses," Nature Communications, Nature, vol. 10(1), pages 1-20, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-09276-w
    DOI: 10.1038/s41467-019-09276-w
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    Cited by:

    1. Junho Kang & Jun Hyeong Lee & Hongui Cha & Jinhyeon An & Joonha Kwon & Seongwoo Lee & Seongryong Kim & Mert Yakup Baykan & So Yeon Kim & Dohyeon An & Ah-Young Kwon & Hee Jung An & Se-Hoon Lee & Jung K, 2024. "Systematic dissection of tumor-normal single-cell ecosystems across a thousand tumors of 30 cancer types," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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