Myeloid Protease-Activated Receptor-2 Contributes to Influenza A Virus Pathology in Mice.
F2rl1
influenza A virus
innate immune response
lung epithelial cell
macrophage
protease-activated receptor 2 (PAR2)
toll-like receptor 3
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
07
10
2021
accepted:
12
11
2021
entrez:
20
12
2021
pubmed:
21
12
2021
medline:
10
2
2022
Statut:
epublish
Résumé
Innate immune responses to influenza A virus (IAV) infection are initiated in part by toll-like receptor 3 (TLR3). TLR3-dependent signaling induces an antiviral immune response and an NFκB-dependent inflammatory response. Protease-activated receptor 2 (PAR2) inhibits the antiviral response and enhances the inflammatory response. PAR2 deficiency protected mice during IAV infection. However, the PAR2 expressing cell-types contributing to IAV pathology in mice and the mechanism by which PAR2 contributes to IAV infection is unknown. IAV infection was analyzed in global ( After IAV infection, Global
Sections du résumé
Background
Innate immune responses to influenza A virus (IAV) infection are initiated in part by toll-like receptor 3 (TLR3). TLR3-dependent signaling induces an antiviral immune response and an NFκB-dependent inflammatory response. Protease-activated receptor 2 (PAR2) inhibits the antiviral response and enhances the inflammatory response. PAR2 deficiency protected mice during IAV infection. However, the PAR2 expressing cell-types contributing to IAV pathology in mice and the mechanism by which PAR2 contributes to IAV infection is unknown.
Methods
IAV infection was analyzed in global (
Results
After IAV infection,
Conclusion
Global
Identifiants
pubmed: 34925374
doi: 10.3389/fimmu.2021.791017
pmc: PMC8671937
doi:
Substances chimiques
Cytokines
0
Receptor, PAR-2
0
Interferon-beta
77238-31-4
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
791017Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL142799
Pays : United States
Organisme : NHLBI NIH HHS
ID : R35 HL155657
Pays : United States
Informations de copyright
Copyright © 2021 Gunther, Bharathi, Miles, Tumey, Schmedes, Tatsumi, Bridges, Martinez, Montgomery, Beck, Camerer, Mackman and Antoniak.
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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