Ifit2 deficiency restricts microglial activation and leukocyte migration following murine coronavirus (m-CoV) CNS infection.
Animals
Apoptosis Regulatory Proteins
/ deficiency
Cell Movement
/ immunology
Coronavirus Infections
/ immunology
Cytokines
/ metabolism
Interferons
/ metabolism
Leukocytes
/ cytology
Mice, Inbred C57BL
Microglia
/ metabolism
Murine hepatitis virus
/ metabolism
RNA-Binding Proteins
/ metabolism
Virus Replication
/ immunology
Journal
PLoS pathogens
ISSN: 1553-7374
Titre abrégé: PLoS Pathog
Pays: United States
ID NLM: 101238921
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
30
06
2020
accepted:
02
10
2020
revised:
15
12
2020
pubmed:
1
12
2020
medline:
30
12
2020
entrez:
30
11
2020
Statut:
epublish
Résumé
The interferon-induced tetratricopeptide repeat protein (Ifit2) protects mice from lethal neurotropic viruses. Neurotropic coronavirus MHV-RSA59 infection of Ifit2-/- mice caused pronounced morbidity and mortality accompanied by rampant virus replication and spread throughout the brain. In spite of the higher virus load, induction of many cytokines and chemokines in the brains of infected Ifit2-/- mice were similar to that in wild-type mice. In contrast, infected Ifit2-/- mice revealed significantly impaired microglial activation as well as reduced recruitment of NK1.1 T cells and CD4 T cells to the brain, possibly contributing to the lack of viral clearance. These two deficiencies were associated with a lower level of microglial expression of CX3CR1, the receptor of the CX3CL1 (Fractalkine) chemokine, which plays a critical role in both microglial activation and leukocyte recruitment. The above results uncovered a new potential role of an interferon-induced protein in immune protection.
Identifiants
pubmed: 33253295
doi: 10.1371/journal.ppat.1009034
pii: PPATHOGENS-D-20-01417
pmc: PMC7738193
doi:
Substances chimiques
Apoptosis Regulatory Proteins
0
Cytokines
0
Ifit2 protein, mouse
0
RNA-Binding Proteins
0
Interferons
9008-11-1
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
e1009034Subventions
Organisme : NCI NIH HHS
ID : R01 CA068782
Pays : United States
Déclaration de conflit d'intérêts
The authors have declared that no competing interests exist.
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