Inflammatory caspases in innate immunity and inflammation.
Détails
ID Serval
serval:BIB_8C76324367B2
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
Inflammatory caspases in innate immunity and inflammation.
Périodique
Journal of Innate Immunity
ISSN
1662-8128[electronic], 1662-811X[linking]
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
2
Numéro
3
Pages
228-237
Langue
anglais
Résumé
Caspases are best known for their role in apoptosis. More recently, they have gained prominence as critical mediators of innate immune responses. The so-called 'inflammatory caspases' include human caspase-1, -4, -5 and -12 and murine caspase-1, -11 and -12. Of these, caspase-1 is best characterized and serves as the prototype for our understanding of the processing, activation and function of inflammatory caspases. Like their apoptotic counterparts, inflammatory caspases are produced as inactive zymogens and require activation to become proteolytically active. Caspase-1 is activated within the inflammasome, a large cytosolic protein complex that is induced by a growing number of endogenous, microbial, chemical or environmental stimuli. The importance of caspase-1 in initiating innate immune responses is demonstrated by its role in cleaving pro-IL-1 beta and pro-IL-18 to their biologically active forms. New functions have also been implicated, as these proteases and the mechanisms underlying their activation and regulation emerge as important mediators of human health and disease.
Mots-clé
Animals, Apoptosis/immunology, Caspases/immunology, Caspases/metabolism, Gene Expression Regulation, Enzymologic, Humans, Immunity, Innate, Inflammation, Inflammation Mediators/immunology, Inflammation Mediators/metabolism, Mice, Protein Processing, Post-Translational
Pubmed
Web of science
Open Access
Oui
Création de la notice
26/11/2010 11:18
Dernière modification de la notice
20/08/2019 14:50