Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice.
anti-inflammatory
dysregulation
immune pathology
interleukin-36γ
liver injury
rift valley fever virus
type I interferon
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2023
2023
Historique:
received:
27
03
2023
accepted:
16
08
2023
medline:
19
9
2023
pubmed:
18
9
2023
entrez:
18
9
2023
Statut:
epublish
Résumé
Type I interferons (IFN) are pro-inflammatory cytokines which can also exert anti-inflammatory effects via the regulation of interleukin (IL)-1 family members. Several studies showed that interferon receptor (IFNAR)-deficient mice develop severe liver damage upon treatment with artificial agonists such as acetaminophen or polyinosinic:polycytidylic acid. In order to investigate if these mechanisms also play a role in an acute viral infection, experiments with the
Identifiants
pubmed: 37720217
doi: 10.3389/fimmu.2023.1194733
pmc: PMC10502725
doi:
Substances chimiques
Interleukin-1
0
Receptor, Interferon alpha-beta
156986-95-7
IL1F9 protein, mouse
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1194733Informations de copyright
Copyright © 2023 Anzaghe, Niles, Korotkova, Dominguez, Kronhart, Ortega Iannazzo, Bechmann, Bachmann, Mühl, Kochs and Waibler.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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