Type I IFN-mediated regulation of IL-1 production in inflammatory disorders.
Détails
Etat: Public
Version: Final published version
Licence: Non spécifiée
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
ID Serval
serval:BIB_A93C669EA17D
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Type I IFN-mediated regulation of IL-1 production in inflammatory disorders.
Périodique
Cellular and Molecular Life Sciences
ISSN
1420-9071 (Electronic)
ISSN-L
1420-682X
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
69
Numéro
20
Pages
3395-3418
Langue
anglais
Résumé
Although contributing to inflammatory responses and to the development of certain autoimmune pathologies, type I interferons (IFNs) are used for the treatment of viral, malignant, and even inflammatory diseases. Interleukin-1 (IL-1) is a strongly pyrogenic cytokine and its importance in the development of several inflammatory diseases is clearly established. While the therapeutic use of IL-1 blocking agents is particularly successful in the treatment of innate-driven inflammatory disorders, IFN treatment has mostly been appreciated in the management of multiple sclerosis. Interestingly, type I IFNs exert multifaceted immunomodulatory effects, including the reduction of IL-1 production, an outcome that could contribute to its efficacy in the treatment of inflammatory diseases. In this review, we summarize the current knowledge on IL-1 and IFN effects in different inflammatory disorders, the influence of IFNs on IL-1 production, and discuss possible therapeutic avenues based on these observations.
Mots-clé
Animals, Humans, Inflammation/drug therapy, Inflammation/metabolism, Interferon Type I/therapeutic use, Interleukin-1/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
18/10/2012 18:06
Dernière modification de la notice
14/02/2022 8:56