期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-07806-6
关键词
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资金
- National Institute of Health Grants (NIH) [AI103338]
- Hirschl Caulier Award
- Canadian Institutes of Health Research [PJT-149023, PJT-152988]
- ARC
- Fondation Bettencourt-Schuller
- American Association of Immunology (AAI)
- NIH [T32A170117]
- Fonds de recherche du Quebec-Sante
- Einstein Cancer Center (NCI cancer center support grant) [2P30CA013330]
Foxp3(+)CD4(+) regulatory T (T-reg) 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 T-reg 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.
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