ER Stress Responses: An Emerging Modulator for Innate Immunity.

Détails

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Etat: Public
Version: Final published version
Licence: CC BY 4.0
ID Serval
serval:BIB_A1E25DB37FD0
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
ER Stress Responses: An Emerging Modulator for Innate Immunity.
Périodique
Cells
Auteur⸱e⸱s
Di Conza G., Ho P.C.
ISSN
2073-4409 (Electronic)
ISSN-L
2073-4409
Statut éditorial
Publié
Date de publication
12/03/2020
Peer-reviewed
Oui
Volume
9
Numéro
3
Pages
695
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review
Publication Status: epublish
Résumé
The endoplasmic reticulum (ER) is a critical organelle, storing the majority of calcium and governing protein translation. Thus, it is crucial to keep the homeostasis in all ER components and machineries. The ER stress sensor pathways, including IRE1/sXBP1, PERK/EIf2 and ATF6, orchestrate the major regulatory circuits to ensure ER homeostasis. The embryonic or postnatal lethality that occurs upon genetic depletion of these sensors reveals the essential role of the ER stress pathway in cell biology. In contrast, the impairment or excessive activation of ER stress has been reported to cause or aggravate several diseases such as atherosclerosis, diabetes, NAFDL/NASH, obesity and cancer. Being part of innate immunity, myeloid cells are the first immune cells entering the inflammation site. Upon entry into a metabolically stressed disease environment, activation of ER stress occurs within the myeloid compartment, leading to the modulation of their phenotype and functions. In this review, we discuss causes and consequences of ER stress activation in the myeloid compartment with a special focus on the crosstalk between ER, innate signaling and metabolic environments.
Mots-clé
Endoplasmic Reticulum Stress/immunology, Humans, Immunity, Innate/immunology, ER stress, chronic diseases, infection, innate immunity
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/04/2020 16:05
Dernière modification de la notice
21/11/2022 8:20
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