Viral infections in humans and mice with genetic deficiencies of the type I IFN response pathway.
Alleles
Animals
Disease Models, Animal
Genetic Predisposition to Disease
Genotype
Humans
Interferon Type I
/ metabolism
Interferon-Stimulated Gene Factor 3, gamma Subunit
/ deficiency
Interferons
/ metabolism
Janus Kinase 1
/ deficiency
Job Syndrome
/ genetics
Mice
Mice, Knockout
Mutation
Phenotype
Receptor, Interferon alpha-beta
/ genetics
STAT1 Transcription Factor
/ deficiency
STAT2 Transcription Factor
/ deficiency
Signal Transduction
TYK2 Kinase
/ deficiency
Virus Diseases
/ etiology
Journal
European journal of immunology
ISSN: 1521-4141
Titre abrégé: Eur J Immunol
Pays: Germany
ID NLM: 1273201
Informations de publication
Date de publication:
05 2021
05 2021
Historique:
revised:
31
01
2021
received:
31
01
2021
accepted:
04
03
2021
pubmed:
18
3
2021
medline:
28
9
2021
entrez:
17
3
2021
Statut:
ppublish
Résumé
Type I IFNs are so-named because they interfere with viral infection in vertebrate cells. The study of cellular responses to type I IFNs led to the discovery of the JAK-STAT signaling pathway, which also governs the response to other cytokine families. We review here the outcome of viral infections in mice and humans with engineered and inborn deficiencies, respectively, of (i) IFNAR1 or IFNAR2, selectively disrupting responses to type I IFNs, (ii) STAT1, STAT2, and IRF9, also impairing cellular responses to type II (for STAT1) and/or III (for STAT1, STAT2, IRF9) IFNs, and (iii) JAK1 and TYK2, also impairing cellular responses to cytokines other than IFNs. A picture is emerging of greater redundancy of human type I IFNs for protective immunity to viruses in natural conditions than was initially anticipated. Mouse type I IFNs are essential for protection against a broad range of viruses in experimental conditions. These findings suggest that various type I IFN-independent mechanisms of human cell-intrinsic immunity to viruses have yet to be discovered.
Identifiants
pubmed: 33729549
doi: 10.1002/eji.202048793
pmc: PMC8900014
mid: NIHMS1780421
doi:
Substances chimiques
IRF9 protein, human
0
Interferon Type I
0
Interferon-Stimulated Gene Factor 3, gamma Subunit
0
STAT1 Transcription Factor
0
STAT1 protein, human
0
STAT2 Transcription Factor
0
Receptor, Interferon alpha-beta
156986-95-7
Interferons
9008-11-1
JAK1 protein, human
EC 2.7.10.2
Janus Kinase 1
EC 2.7.10.2
TYK2 Kinase
EC 2.7.10.2
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1039-1061Subventions
Organisme : NIAID NIH HHS
ID : R01 AI095983
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI151663
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001866
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI143810
Pays : United States
Organisme : Howard Hughes Medical Institute
Pays : United States
Organisme : NIAID NIH HHS
ID : R21 AI137371
Pays : United States
Organisme : NIAID NIH HHS
ID : R37 AI095983
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI088364
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI127564
Pays : United States
Organisme : NHGRI NIH HHS
ID : U24 HG008956
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS072381
Pays : United States
Organisme : NHGRI NIH HHS
ID : UM1 HG006504
Pays : United States
Informations de copyright
© 2021 Wiley-VCH GmbH.
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