Innate immune recognition of francisella tularensis: activation of type-I interferons and the inflammasome.

Détails

Ressource 1Télécharger: fmicb-02-00016.pdf (1693.26 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_74385AAE11FA
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Innate immune recognition of francisella tularensis: activation of type-I interferons and the inflammasome.
Périodique
Frontiers in Microbiology
Auteur(s)
Jones J.W., Broz P., Monack D.M.
ISSN
1664-302X (Electronic)
ISSN-L
1664-302X
Statut éditorial
Publié
Date de publication
2011
Peer-reviewed
Oui
Volume
2
Pages
16
Langue
anglais
Résumé
Francisella tularensis is an intracellular pathogen that can cause severe disease in a wide range of mammalian hosts. Primarily residing in host macrophages, F. tularensis escapes phagosomal degradation, and replicates in the macrophage cytosol. The macrophage uses a series of pattern recognition receptors to detect conserved microbial molecules from invading pathogens, and initiates an appropriate host response. In the cytosol, F. tularensis is recognized by the inflammasome, a multiprotein complex responsible for the activation of the cysteine protease caspase-1. Caspase-1 activation leads to processing and release of proinflammatory cytokines and host cell death. Here we review recent work on the molecular mechanisms of inflammasome activation by F. tularensis, and its consequences both in vitro and in vivo. Finally, we discuss the coordination between the inflammasome and other cytosolic host responses, and the evidence for F. tularensis virulence factors that suppress inflammasome activation.

Mots-clé
Aim2, Asc, Francisella, Sting, caspase-1, inflammasome, interferon, interleukin-1b, AIM2, ASC, STING
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/10/2017 10:05
Dernière modification de la notice
20/08/2019 14:31
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