Intercellular Communication Is Key for Protective IFNα/β Signaling During Viral Central Nervous System Infection.
IFN
IFN/
astrocytes
viral encephalitis
Journal
Viral immunology
ISSN: 1557-8976
Titre abrégé: Viral Immunol
Pays: United States
ID NLM: 8801552
Informations de publication
Date de publication:
Historique:
pubmed:
18
9
2018
medline:
21
5
2019
entrez:
18
9
2018
Statut:
ppublish
Résumé
A variety of viruses can induce central nervous system (CNS) infections and neurological diseases, although the incidence is rare. Similar to peripheral infections, IFNα/β induction and signaling constitutes a first line of defense to limit virus dissemination. However, CNS-resident cells differ widely in their repertoire and magnitude of both basal and inducible components in the IFNα/β pathway. While microglia as resident myeloid cells have been implicated as prominent sentinels of CNS invading pathogens or insults, astrocytes are emerging as key responders to many neurotropic RNA virus infections. Focusing on RNA viruses, this review discusses the role of astrocytes as IFNα/β inducers and responders and touches on the role of IFNα/β receptor signaling in regulating myeloid cell activation and IFNγ responsiveness. A summary picture emerges implicating IFNα/β not only as key in establishing the classical "antiviral" state, but also orchestrating cell mobility and IFNγ-mediated effector functions.
Identifiants
pubmed: 30222502
doi: 10.1089/vim.2018.0101
pmc: PMC6350053
doi:
Substances chimiques
Interferon-alpha
0
Interferon-beta
77238-31-4
Interferon-gamma
82115-62-6
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-6Subventions
Organisme : NINDS NIH HHS
ID : P01 NS064932
Pays : United States
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