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Trained immunity in viral infections, Alzheimer's disease and multiple sclerosis: A convergence in type I interferon signalling and IFNβ-1a

Thumbnail
Autor
Vavougios G.D., Mavridis T., Artemiadis A., Krogfelt K.A., Hadjigeorgiou G.
Fecha
2022
Language
en
DOI
10.1016/j.bbadis.2022.166430
Materia
beta1a interferon
interferon inducible transmembrane protein 3
membrane protein
oligoadenylate synthetase 1
unclassified drug
beta interferon
Alzheimer disease
coronavirus disease 2019
epigenetics
human
immunological memory
immunomodulation
innate immunity
multiple sclerosis
nervous system inflammation
Review
type I interferon signaling
virus immunity
virus infection
Alzheimer Disease
COVID-19
Humans
Interferon-beta
Multiple Sclerosis
Virus Diseases
Elsevier B.V.
Mostrar el registro completo del ítem
Resumen
Type I interferon (IFN-I) signalling represents a major target for modulation in a virus' bid for latency. IFN-I perturbations are also present in such as Alzheimer's disease (AD) and multiple sclerosis (MS), where viral infections are known to increase symptomatic burden. IFN-I modulation such as via IFNβ-1a, an established MS treatment, has been researched to a limited extent to both AD and COVID-19. In this mini review, we present emerging research on trained immunity as a pathogenetic basis for Alzheimer's disease and the emerging context for IFNβ-1a repositioning, via mechanisms shared with multiple sclerosis and induced by viral infections. © 2022 Elsevier B.V.
URI
http://hdl.handle.net/11615/80532
Colecciones
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]

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