β-Catenin Signaling Drives Differentiation and Proinflammatory Function of IRF8-Dependent Dendritic Cells.

Détails

Ressource 1Télécharger: BIB_BA9728A16A7E.P001.pdf (2552.12 [Ko])
Etat: Public
Version: de l'auteur
ID Serval
serval:BIB_BA9728A16A7E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
β-Catenin Signaling Drives Differentiation and Proinflammatory Function of IRF8-Dependent Dendritic Cells.
Périodique
Journal of Immunology
Auteur(s)
Cohen S.B., Smith N.L., McDougal C., Pepper M., Shah S., Yap G.S., Acha-Orbea H., Jiang A., Clausen B.E., Rudd B.D., Denkers E.Y.
ISSN
1550-6606 (Electronic)
ISSN-L
0022-1767
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
194
Numéro
1
Pages
210-222
Langue
anglais
Résumé
β-Catenin signaling has recently been tied to the emergence of tolerogenic dendritic cells (DCs). In this article, we demonstrate a novel role for β-catenin in directing DC subset development through IFN regulatory factor 8 (IRF8) activation. We found that splenic DC precursors express β-catenin, and DCs from mice with CD11c-specific constitutive β-catenin activation upregulated IRF8 through targeting of the Irf8 promoter, leading to in vivo expansion of IRF8-dependent CD8α(+), plasmacytoid, and CD103(+)CD11b(-) DCs. β-Catenin-stabilized CD8α(+) DCs secreted elevated IL-12 upon in vitro microbial stimulation, and pharmacological β-catenin inhibition blocked this response in wild-type cells. Upon infections with Toxoplasma gondii and vaccinia virus, mice with stabilized DC β-catenin displayed abnormally high Th1 and CD8(+) T lymphocyte responses, respectively. Collectively, these results reveal a novel and unexpected function for β-catenin in programming DC differentiation toward subsets that orchestrate proinflammatory immunity to infection.
Pubmed
Web of science
Open Access
Oui
Création de la notice
16/12/2014 14:38
Dernière modification de la notice
20/08/2019 16:28
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