ER Stress Responses: An Emerging Modulator for Innate Immunity.

Details

Serval ID
serval:BIB_A1E25DB37FD0
Type
Article: article from journal or magazin.
Publication sub-type
Review (review): journal as complete as possible of one specific subject, written based on exhaustive analyses from published work.
Collection
Publications
Institution
Title
ER Stress Responses: An Emerging Modulator for Innate Immunity.
Journal
Cells
Author(s)
Di Conza G., Ho P.C.
ISSN
2073-4409 (Electronic)
ISSN-L
2073-4409
Publication state
Published
Issued date
12/03/2020
Peer-reviewed
Oui
Volume
9
Number
3
Language
english
Notes
Publication types: Journal Article ; Review
Publication Status: epublish
Abstract
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.
Keywords
ER stress, chronic diseases, infection, innate immunity
Pubmed
Open Access
Yes
Create date
02/04/2020 17:05
Last modification date
09/09/2020 6:26
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