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Interleukin 2 modulates thymic-derived regulatory T cell epigenetic landscape

Author

Listed:
  • Laurent Chorro

    (Albert Einstein College of Medicine)

  • Masako Suzuki

    (Albert Einstein College of Medicine)

  • Shu Shien Chin

    (Albert Einstein College of Medicine)

  • Tere M. Williams

    (Albert Einstein College of Medicine)

  • Erik L. Snapp

    (Albert Einstein College of Medicine
    Janelia Research Campus of the Howard Hughes Medical Institute)

  • Livia Odagiu

    (University of Montreal)

  • Nathalie Labrecque

    (University of Montreal)

  • Grégoire Lauvau

    (Albert Einstein College of Medicine)

Abstract

Foxp3+CD4+ regulatory T (Treg) cells are essential for preventing fatal autoimmunity and safeguard immune homeostasis in vivo. While expression of the transcription factor Foxp3 and IL-2 signals are both required for the development and function of Treg cells, the commitment to the Treg cell lineage occurs during thymic selection upon T cell receptor (TCR) triggering, and precedes the expression of Foxp3. Whether signals beside TCR contribute to establish Treg cell epigenetic and functional identity is still unknown. Here, using a mouse model with reduced IL-2 signaling, we show that IL-2 regulates the positioning of the pioneer factor SATB1 in CD4+ thymocytes and controls genome wide chromatin accessibility of thymic-derived Treg cells. We also show that Treg cells receiving only low IL-2 signals can suppress endogenous but not WT autoreactive T cell responses in vitro and in vivo. Our findings have broad implications for potential therapeutic strategies to reprogram Treg cells in vivo.

Suggested Citation

  • Laurent Chorro & Masako Suzuki & Shu Shien Chin & Tere M. Williams & Erik L. Snapp & Livia Odagiu & Nathalie Labrecque & Grégoire Lauvau, 2018. "Interleukin 2 modulates thymic-derived regulatory T cell epigenetic landscape," Nature Communications, Nature, vol. 9(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07806-6
    DOI: 10.1038/s41467-018-07806-6
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