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WeightNameValue
1000 Titel
  • Central immune tolerance depends on crosstalk between the classical and alternative NF-κB pathways in medullary thymic epithelial cells
1000 Autor/in
  1. Riemann, Marc |
  2. Andreas, Nico |
  3. Fedoseeva, Maria |
  4. Meier, Elke |
  5. Weih, Debra |
  6. Freytag, Helga |
  7. Schmidt-Ullrich, Ruth |
  8. Klein, Ulf |
  9. wang, zhao-qi |
  10. Weih, Falk |
1000 Erscheinungsjahr 2017
1000 LeibnizOpen
1000 Art der Datei
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2017-04-03
1000 Erschienen in
1000 Quellenangabe
  • 81:56-67
1000 FRL-Sammlung
1000 Copyrightjahr
  • 2017
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.1016/j.jaut.2017.03.007 |
1000 Ergänzendes Material
  • https://www.sciencedirect.com/science/article/pii/S0896841116303997?via%3Dihub#appsec1 |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Sprache der Publikation
1000 Abstract/Summary
  • Medullary thymic epithelial cells (mTECs) contribute to self-tolerance by expressing and presenting peripheral tissue antigens for negative selection of autoreactive T cells and differentiation of natural regulatory T cells. The molecular control of mTEC development remains incompletely understood. We here demonstrate by TEC-specific gene manipulation in mice that the NF-κB transcription factor subunit RelB, which is activated by the alternative NF-κB pathway, regulates development of mature mTECs in a dose-dependent manner. Mice with conditional deletion of Relb lacked mature mTECs and developed spontaneous autoimmunity. In addition, the NF-κB subunits RelA and c-Rel, which are both activated by classical NF-κB signaling, were jointly required for mTEC differentiation by directly regulating the transcription of Relb. Our data reveal a crosstalk mechanism between classical and alternative NF-κB pathways that tightly controls the development of mature mTECs to ensure self-tolerance.
1000 Sacherschließung
lokal Autoimmunity
lokal NF-κB
lokal Central immune tolerance
lokal Medullary thymic epithelial cells
lokal Conditional gene targeting
1000 Fachgruppe
  1. Medizin |
  2. Biologie |
1000 Fächerklassifikation (DDC)
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/creator/UmllbWFubiwgTWFyYw==|https://frl.publisso.de/adhoc/creator/QW5kcmVhcywgTmljbw==|https://frl.publisso.de/adhoc/creator/RmVkb3NlZXZhLCBNYXJpYQ==|https://frl.publisso.de/adhoc/creator/TWVpZXIsIEVsa2U=|https://frl.publisso.de/adhoc/creator/V2VpaCwgRGVicmE=|https://frl.publisso.de/adhoc/creator/RnJleXRhZywgSGVsZ2E=|https://orcid.org/0000-0002-2472-6530|https://frl.publisso.de/adhoc/creator/S2xlaW4sIFVsZg==|https://orcid.org/0000-0002-8336-3485|https://frl.publisso.de/adhoc/creator/V2VpaCwgRmFsaw==
1000 Förderer
  1. Deutsche Forschungsgemeinschaft |
  2. Leibniz Institute on Aging, Fritz Lipmann Institute (FLI), Jena |
1000 Fördernummer
  1. WE 2224/6; WE 2224/6-2
  2. -
1000 Förderprogramm
  1. -
  2. Open access charge
1000 Dateien
1000 Förderung
  1. 1000 joinedFunding-child
    1000 Förderer Deutsche Forschungsgemeinschaft |
    1000 Förderprogramm -
    1000 Fördernummer WE 2224/6; WE 2224/6-2
  2. 1000 joinedFunding-child
    1000 Förderer Leibniz Institute on Aging, Fritz Lipmann Institute (FLI), Jena |
    1000 Förderprogramm Open access charge
    1000 Fördernummer -
1000 Objektart article
1000 Beschrieben durch
1000 @id frl:6413732.rdf
1000 Erstellt am 2019-04-02T15:14:30.847+0200
1000 Erstellt von 285
1000 beschreibt frl:6413732
1000 Bearbeitet von 25
1000 Zuletzt bearbeitet Mon Apr 08 10:34:05 CEST 2019
1000 Objekt bearb. Mon Apr 08 10:31:54 CEST 2019
1000 Vgl. frl:6413732
1000 Oai Id
  1. oai:frl.publisso.de:frl:6413732 |
1000 Sichtbarkeit Metadaten public
1000 Sichtbarkeit Daten public
1000 Gegenstand von

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