{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:10:29Z","timestamp":1791295829317,"version":"4.1.0"},"reference-count":77,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2012,11,1]],"date-time":"2012-11-01T00:00:00Z","timestamp":1351728000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2012,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>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-\u03b2 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\u2013glucose 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\u2013glucose 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-\u03b2 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.<\/jats:p>","DOI":"10.4049\/jimmunol.1102737","type":"journal-article","created":{"date-parts":[[2012,10,2]],"date-time":"2012-10-02T06:18:13Z","timestamp":1349158693000},"page":"4630-4639","source":"Crossref","is-referenced-by-count":137,"title":["Endoplasmic Reticulum Stress Regulates the Innate Immunity Critical Transcription Factor IRF3"],"prefix":"10.1093","volume":"189","author":[{"given":"Yi-Ping","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ling","family":"Zeng","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Austin","family":"Tian","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ashley","family":"Bomkamp","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Rivera","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Delia","family":"Gutman","sequence":"additional","affiliation":[{"name":"Department of Medicine, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, University of Miami , Miami, FL 33136"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Glen N","family":"Barber","sequence":"additional","affiliation":[{"name":"Department of Medicine, Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, University of Miami , Miami, FL 33136"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie K","family":"Olson","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Judith A","family":"Smith","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin , Madison, WI 53792"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,11,1]]},"reference":[{"key":"2025032409322060200_r1","doi-asserted-by":"crossref","first-page":"307","DOI":"10.1146\/annurev.immunol.23.021704.115843","article-title":"Type I interferons (alpha\/beta) in immunity and autoimmunity","volume":"23","author":"Theofilopoulos","year":"2005","journal-title":"Annu. 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