RelB suppresses type I Interferon signaling in dendritic cells.
Amino Acid Sequence
Animals
Cell Differentiation
Cells, Cultured
Crosses, Genetic
Dendritic Cells
/ classification
Gene Expression Regulation
/ immunology
Interferon Type I
/ immunology
Mice
NF-KappaB Inhibitor alpha
/ physiology
NIH 3T3 Cells
Newcastle disease virus
/ immunology
Peptides
/ pharmacology
Receptor, Interferon alpha-beta
/ deficiency
Signal Transduction
/ immunology
Spleen
/ cytology
Transcription Factor RelB
/ deficiency
Viral Load
Dendritic cell differentiation
Interferon stimulated genes (ISGs)
NF-κB signaling
RelB
Type I Interferon (IFN)
Journal
Cellular immunology
ISSN: 1090-2163
Titre abrégé: Cell Immunol
Pays: Netherlands
ID NLM: 1246405
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
26
09
2019
revised:
23
12
2019
accepted:
10
01
2020
pubmed:
12
2
2020
medline:
18
8
2020
entrez:
12
2
2020
Statut:
ppublish
Résumé
Type I Interferon (IFN) signaling plays a critical role in dendritic cell (DC) development and functions. Inhibition of hyper type I IFN signaling promotes cDC2 subtype development. Relb is essential to development of cDC2 subtype and here we analyzed its effect on type I IFN signaling in DCs. We show that Relb suppresses the homeostatic type I IFN signaling in cDC2 cultures. TLR stimulation of FL-DCs led to RelB induction coinciding with fall in IFN signatures; conforming with the observation Relb expression reduced TLR stimulated IFN induction along with decrease in ISGs. Towards understanding mechanism, we show that effects of RelB are mediated by increased levels of IκBα. We demonstrate that RelB dampened antiviral responses by lowering ISG levels and the defect in cDC2 development in RelB null mice can be rescued in Ifnar1
Identifiants
pubmed: 32044112
pii: S0008-8749(19)30399-5
doi: 10.1016/j.cellimm.2020.104043
pii:
doi:
Substances chimiques
Ifnar1 protein, mouse
0
Interferon Type I
0
Peptides
0
Relb protein, mouse
0
SN52 peptide
0
NF-KappaB Inhibitor alpha
139874-52-5
Transcription Factor RelB
147337-75-5
Receptor, Interferon alpha-beta
156986-95-7
Types de publication
Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
104043Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.