期刊
CELL REPORTS
卷 20, 期 12, 页码 2906-2920出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.08.068
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资金
- NHMRC [1069075, 1106378, 1054925, 1127198]
- Sylvia and Charles Viertel Foundation
- Walter and Eliza Institute - CSL
- Landsteiner Foundation for Blood Transfusion Research (LSBR) [1014]
- Center of Immunodeficiencies Amsterdam
- Kidney Health Australia
- Australian Government
- National Health and Medical Research Council of Australia [1127198, 1106378, 1069075] Funding Source: NHMRC
After exiting the thymus, Foxp3(+) regulatory T (Treg) cells undergo further differentiation in the periphery, resulting in the generation of mature, fully suppressive effector (e) Treg cells in a process dependent on TCR signaling and the transcription factor IRF4. Here, we show that tumor necrosis factor receptor superfamily (TNFRSF) signaling plays a crucial role in the development and maintenance of eTreg cells. TNFRSF signaling activated the NF-kappa B transcription factor RelA, which was required to maintain eTreg cells in lymphoid and non-lymphoid tissues, including ROR gamma t(+) Treg cells in the small intestine. In response to TNFRSF signaling, RelA regulated basic cellular processes, including cell survival and proliferation, but was dispensable for IRF4 expression or DNAbinding, indicating that both pathways operated independently. Importantly, mutations in the RelA binding partner NF-kappa B1 compromised eTreg cells in humans, suggesting that the TNFRSF-NF-kappa B axis was required in a non-redundant manner to maintain eTreg cells in mice and humans.
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