Interleukin 2 modulates thymic-derived regulatory T cell epigenetic landscape

Laurent Chorro, Masako Suzuki, Shu Shien Chin, Tere M. Williams, Erik L. Snapp, Livia Odagiu, Nathalie Labrecque and Grégoire Lauvau ()
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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
Livia Odagiu: University of Montreal
Nathalie Labrecque: University of Montreal
Grégoire Lauvau: Albert Einstein College of Medicine

Nature Communications, 2018, vol. 9, issue 1, 1-17

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-07806-6

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