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The NF-κB RelA Transcription Factor Is Critical for Regulatory T Cell Activation and Stability

Authors
  • Ronin, Emilie1
  • Lubrano di Ricco, Martina1
  • Vallion, Romain1
  • Divoux, Jordane1
  • Kwon, Ho-Keun2
  • Grégoire, Sylvie1
  • Collares, Davi3
  • Rouers, Angéline1
  • Baud, Véronique3
  • Benoist, Christophe2
  • Salomon, Benoit L.1
  • 1 Sorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses (CIMI-Paris), Paris , (France)
  • 2 Division of Immunology, Department of Microbiology and Immunobiology, Harvard Medical School, Boston, MA , (United States)
  • 3 Laboratoire NF-κB, Differentiation and Cancer, Université Paris Descartes, Sorbonne Paris Cité, Paris , (France)
Type
Published Article
Journal
Frontiers in Immunology
Publisher
Frontiers Media SA
Publication Date
Oct 30, 2019
Volume
10
Identifiers
DOI: 10.3389/fimmu.2019.02487
Source
Frontiers
Keywords
Disciplines
  • Immunology
  • Original Research
License
Green

Abstract

Regulatory T cells (Tregs) play a major role in immune homeostasis and in the prevention of autoimmune diseases. It has been shown that c-Rel is critical in Treg thymic differentiation, but little is known on the role of NF-κB on mature Treg biology. We thus generated mice with a specific knockout of RelA, a key member of NF-κB, in Tregs. These mice developed a severe autoimmune syndrome with multi-organ immune infiltration and high activation of lymphoid and myeloid cells. Phenotypic and transcriptomic analyses showed that RelA is critical in the acquisition of the effector Treg state independently of surrounding inflammatory environment. Unexpectedly, RelA-deficient Tregs also displayed reduced stability and cells that had lost Foxp3 produced inflammatory cytokines. Overall, we show that RelA is critical for Treg biology as it promotes both the generation of their effector phenotype and the maintenance of their identity.

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