NDLI: Endoplasmic reticulum stress regulates the innate immunity critical transcription factor IRF3.

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Endoplasmic reticulum stress regulates the innate immunity critical transcription factor IRF3.

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Endoplasmic reticulum stress regulates the innate immunity critical transcription factor IRF3.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tian, Austin Olson, Julie K. Barber, Glen N. Smith, Judith A. Liu, Yi-Ping Bomkamp, Ashley Gutman, Delia Zeng, Ling Rivera, Daniel
Description	Country affiliation: United States Author Affiliation: Liu YP ( Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin, Madison, WI 53792, USA.)
Abstract	IFN regulatory factor 3 (IRF3) regulates early type I IFNs and other genes involved in innate immunity. We have previously shown that cells undergoing an endoplasmic reticulum (ER) stress response called the unfolded protein response produce synergistically augmented IFN-ß when stimulated with pattern recognition receptor agonists such as LPS. Concomitant ER stress and LPS stimulation resulted in greater recruitment of the IRF3 transcription factor to ifnb1 gene regulatory elements. In this study, we used murine cells to demonstrate that both oxygen-glucose deprivation and pharmacologic unfolded protein response inducers trigger phosphorylation and nuclear translocation of IRF3, even in the absence of exogenous LPS. Different ER stressors used distinct mechanisms to activate IRF3: IRF3 phosphorylation due to calcium-mobilizing ER stress (thapsigargin treatment, oxygen-glucose deprivation) critically depended upon stimulator of IFN gene, an ER-resident nucleic acid-responsive molecule. However, calcium mobilization alone by ionomycin was insufficient for IRF3 phosphorylation. In contrast, other forms of ER stress (e.g., tunicamycin treatment) promote IRF3 phosphorylation independently of stimulator of IFN gene and TANK-binding kinase 1. Rather, IRF3 activation by tunicamycin and 2-deoxyglucose was inhibited by 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride, a serine protease inhibitor that blocks activating transcription factor 6 processing. Interfering with ER stress-induced IRF3 activation abrogated IFN-ß synergy. Together, these data suggest ER stress primes cells to respond to innate immune stimuli by activating the IRF3 transcription factor. Our results also suggest certain types of ER stress accomplish IRF3 phosphorylation by co-opting existing innate immune pathogen response pathways. These data have implications for diseases involving ER stress and type I IFN.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1102737
Journal	The Journal of Immunology
Issue Number	9
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Endoplasmic Reticulum Stress Immunology Immunity, Innate Interferon Regulatory Factor-3 Metabolism Active Transport, Cell Nucleus Drug Effects Animals Calcium Signaling Cell Line Lactones Pharmacology Lipopolysaccharides Physiology Membrane Proteins Deficiency Genetics Mice Mice, Inbred C57bl Mice, Knockout Phosphorylation Protein-serine-threonine Kinases Sesquiterpenes Unfolded Protein Response Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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