ICER is requisite for Th17 differentiation.
Détails
Télécharger: ncomms12993.pdf (1906.90 [Ko])
Etat: Public
Version: de l'auteur⸱e
Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_A6AFD41C6AE7
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
ICER is requisite for Th17 differentiation.
Périodique
Nature Communications
ISSN
2041-1723 (Electronic)
ISSN-L
2041-1723
Statut éditorial
Publié
Date de publication
2016
Peer-reviewed
Oui
Volume
7
Pages
12993
Langue
anglais
Notes
Publication types: ARTICLE
Publication Status: epublish
Publication Status: epublish
Résumé
Inducible cAMP early repressor (ICER) has been described as a transcriptional repressor isoform of the cAMP response element modulator (CREM). Here we report that ICER is predominantly expressed in Th17 cells through the IL-6-STAT3 pathway and binds to the Il17a promoter, where it facilitates the accumulation of the canonical enhancer RORγt. In vitro differentiation from naive ICER/CREM-deficient CD4(+) T cells to Th17 cells is impaired but can be rescued by forced overexpression of ICER. Consistent with a role of Th17 cells in autoimmune and inflammatory diseases, ICER/CREM-deficient B6.lpr mice are protected from developing autoimmunity. Similarly, both anti-glomerular basement membrane-induced glomerulonephritis and experimental encephalomyelitis are attenuated in ICER/CREM-deficient mice compared with their ICER/CREM-sufficient littermates. Importantly, we find ICER overexpressed in CD4(+) T cells from patients with systemic lupus erythematosus. Collectively, our findings identify a unique role for ICER, which affects both organ-specific and systemic autoimmunity in a Th17-dependent manner.
Pubmed
Web of science
Open Access
Oui
Création de la notice
11/10/2016 18:56
Dernière modification de la notice
20/08/2019 16:11