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Conserved human effector Treg cell transcriptomic and epigenetic signature in arthritic joint inflammation

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Listed:
  • Gerdien Mijnheer

    (University Medical Center Utrecht, Utrecht University)

  • Lisanne Lutter

    (University Medical Center Utrecht, Utrecht University)

  • Michal Mokry

    (University Medical Center Utrecht, Utrecht University
    University Medical Center Utrecht
    University Medical Center Utrecht)

  • Marlot Wal

    (University Medical Center Utrecht, Utrecht University)

  • Rianne Scholman

    (University Medical Center Utrecht, Utrecht University)

  • Veerle Fleskens

    (School of Immunology & Microbial Sciences, King’s College London)

  • Aridaman Pandit

    (University Medical Center Utrecht, Utrecht University)

  • Weiyang Tao

    (University Medical Center Utrecht, Utrecht University)

  • Mark Wekking

    (University Medical Center Utrecht)

  • Stephin Vervoort

    (University Medical Center Utrecht, Utrecht University
    University Medical Center Utrecht)

  • Ceri Roberts

    (School of Immunology & Microbial Sciences, King’s College London)

  • Alessandra Petrelli

    (University Medical Center Utrecht, Utrecht University)

  • Janneke G. C. Peeters

    (University Medical Center Utrecht, Utrecht University)

  • Marthe Knijff

    (University Medical Center Utrecht, Utrecht University)

  • Sytze Roock

    (University Medical Center Utrecht, Utrecht University)

  • Sebastiaan Vastert

    (University Medical Center Utrecht, Utrecht University)

  • Leonie S. Taams

    (School of Immunology & Microbial Sciences, King’s College London)

  • Jorg Loosdregt

    (University Medical Center Utrecht, Utrecht University
    University Medical Center Utrecht)

  • Femke Wijk

    (University Medical Center Utrecht, Utrecht University)

Abstract

Treg cells are critical regulators of immune homeostasis, and environment-driven Treg cell differentiation into effector (e)Treg cells is crucial for optimal functioning. However, human Treg cell programming in inflammation is unclear. Here, we combine transcriptional and epigenetic profiling to identify a human eTreg cell signature. Inflammation-derived functional Treg cells have a transcriptional profile characterized by upregulation of both a core Treg cell (FOXP3, CTLA4, TIGIT) and effector program (GITR, BLIMP-1, BATF). We identify a specific human eTreg cell signature that includes the vitamin D receptor (VDR) as a predicted regulator in eTreg cell differentiation. H3K27ac/H3K4me1 occupancy indicates an altered (super-)enhancer landscape, including enrichment of the VDR and BATF binding motifs. The Treg cell profile has striking overlap with tumor-infiltrating Treg cells. Our data demonstrate that human inflammation-derived Treg cells acquire a conserved and specific eTreg cell profile guided by epigenetic changes, and fine-tuned by environment-specific adaptations.

Suggested Citation

  • Gerdien Mijnheer & Lisanne Lutter & Michal Mokry & Marlot Wal & Rianne Scholman & Veerle Fleskens & Aridaman Pandit & Weiyang Tao & Mark Wekking & Stephin Vervoort & Ceri Roberts & Alessandra Petrelli, 2021. "Conserved human effector Treg cell transcriptomic and epigenetic signature in arthritic joint inflammation," Nature Communications, Nature, vol. 12(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-22975-7
    DOI: 10.1038/s41467-021-22975-7
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    Cited by:

    1. Lanqi Gong & Jie Luo & Yu Zhang & Yuma Yang & Shanshan Li & Xiaona Fang & Baifeng Zhang & Jiao Huang & Larry Ka-Yue Chow & Dittman Chung & Jinlin Huang & Cuicui Huang & Qin Liu & Lu Bai & Yuen Chak Ti, 2023. "Nasopharyngeal carcinoma cells promote regulatory T cell development and suppressive activity via CD70-CD27 interaction," Nature Communications, Nature, vol. 14(1), pages 1-24, December.

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