ICER is requisite for Th17 differentiation.

Détails

Ressource 1Télécharger: ncomms12993.pdf (1906.90 [Ko])
Etat: Public
Version: de l'auteur
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
Auteur(s)
Yoshida N., Comte D., Mizui M., Otomo K., Rosetti F., Mayadas T.N., Crispín J.C., Bradley S.J., Koga T., Kono M., Karampetsou M.P., Kyttaris V.C., Tenbrock K., Tsokos G.C.
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
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
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