Cited by 296interferon and immune responsesImmune Response and InflammationImmunotherapy and Immune Responses

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IRF-3, IRF-5, and IRF-7 Coordinately Regulate the Type I IFN Response in Myeloid Dendritic Cells Downstream of MAVS Signaling

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Lazear, Helen M., Lancaster, Alissa, Wilkins, Courtney, Suthar, Mehul S., Huang, Albert, Vick, Sarah C., Clepper, Lisa, Thackray, Larissa, Brassil, Margaret M., Virgin, Herbert W., Nikolich-Zugich, Janko, Moses, Ashlee V., Gale, Michael, Früh, Klaus, Diamond, Michael S.·2013·PLoS Pathogens

DOI 10.1371/journal.ppat.1003118PMC PMC3536698

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Abstract

Although the transcription factors IRF-3 and IRF-7 are considered master regulators of type I interferon (IFN) induction and IFN stimulated gene (ISG) expression, Irf3(-/-)×Irf7(-/-) double knockout (DKO) myeloid dendritic cells (mDC) produce relatively normal levels of IFN-β after viral infection. We generated Irf3(-/-)×Irf5(-/-)×Irf7(-/-) triple knockout (TKO) mice to test whether IRF-5 was the source of the residual induction of IFN-β and ISGs in mDCs. In pathogenesis studies with two unrelated positive-sense RNA viruses (West Nile virus (WNV) and murine norovirus), TKO mice succumbed at rates greater than DKO mice and equal to or approaching those of mice lacking the type I IFN receptor (Ifnar(-/-)). In ex vivo studies, after WNV infection or exposure to Toll-like receptor agonists, TKO mDCs failed to produce IFN-β or express ISGs. In contrast, this response was sustained in TKO macrophages following WNV infection. To define IRF-regulated gene signatures, we performed microarray analysis on WNV-infected mDC from wild type (WT), DKO, TKO, or Ifnar(-/-) mice, as well as from mice lacking the RIG-I like receptor adaptor protein MAVS. Whereas the gene induction pattern in DKO mDC was similar to WT cells, remarkably, almost no ISG induction was detected in TKO or Mavs(-/-) mDC. The relative equivalence of TKO and Mavs(-/-) responses suggested that MAVS dominantly regulates ISG induction in mDC. Moreover, we showed that MAVS-dependent induction of ISGs can occur through an IRF-5-dependent yet IRF-3 and IRF-7-independent pathway. Our results establish IRF-3, -5, and -7 as the key transcription factors responsible for mediating the type I IFN and ISG response in mDC during WNV infection and suggest a novel signaling link between MAVS and IRF-5.

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Mitochondria and Antiviral Immunity
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BackgroundSelf-citation
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“I induction predominate (37, 39, 40).”
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Background
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“7 the related IRF7 are expressed in neuronal cells (53,54), we cannot rule out the possibility that cGAS may induce these targets depending upon the cell types in HD.”
Background
Loss of Neuroligin 4X Induces an Intrinsic Innate Immune Response in TNBCPreprint
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“mitochondrial antiviral signaling protein (MAVS) was distinguished in mice [11].”
Background
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“…cells with PolyIC stimulus produce a little IFN β , though the weaker IRF-inducing stimulus LPS shows no IFN β induction even in this double ko (26–29). κ In contrast, NF Bko cells, which lack subunits RelA and cRel, show severely diminished IFN β expression when LPS is the stimulus, while they…”
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“…ª 2017 Elsevier Inc. 305 (Ifnar1 / ), mice that lack transcription factors required for IFN-a/b production (Irf3 / 3 Irf5 / 3 Irf7 / ), and mice with defective pattern recognition receptor signaling (Mavs / ), all of which succumb rapidly to WNV infection (Lazear et al., 2013; Suthar et al., 2010).”
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Authors: Lazear, H. M., Lancaster, A., Wilkins, C., Suthar, M. S., Huang, A., Vick, S. C., Clepper, L., Thackray, L., Brassil, M. M., Virgin, H. W., Nikolich-Zugich, J., Moses, A. V., Gale, M., Früh, K., & Diamond, M. S.
Affiliations: Washington University in St. Louis (US)
Oregon Health & Science University (US)
University of Washington (US)
Emory University (US)
Vaccine and Gene Therapy Institute (US)
Corresponding author: Diamond, Michael S.
ORCID: Lazear, Helen M.
Wilkins, Courtney
Suthar, Mehul S.
Huang, Albert
Vick, Sarah C.
Thackray, Larissa
Virgin, Herbert W.
Moses, Ashlee V.
Gale, Michael
Früh, Klaus
Diamond, Michael S.
Venue: PLoS Pathogens
Publisher: Public Library of Science (PLoS)
Published: 2013-01-03
Volume: 9
Issue: 1
Pages: e1003118
ISSN: 1553-7366 (ISSN-L)
1553-7374
DOI: 10.1371/journal.ppat.1003118
PMC: PMC3536698
OpenAlex: W2036679352
Cited by: 296
References: 85
Citations by year: 2026: 7 · 2025: 11 · 2024: 12 · 2023: 11 · 2022: 21 · 2021: 25 · 2020: 27 · 2019: 22 · 2018: 30 · 2017: 25 · 2016: 28 · 2015: 20 · 2014: 33 · 2013: 23
FWCI: 19.19
Type: journal article
Language: en
Update notices: correction (2013-05-03)
Open access: gold
doi.org
Licence: cc-by
creativecommons.org/licenses/by/4.0/ (unspecified)
Locations: PLoS Pathogens (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
Digital Commons@Becker (Washington University School of Medicine) (submittedVersion)
Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Figshare (submittedVersion, cc-by)
UNC Libraries
Funders: National Institutes of Health (n01ai50027-8-0-1, AI083019, AI057160)
National Institute of Allergy and Infectious Diseases (N01 AI50027, U19AI083019, U54AI081680, N01 AI050027, R01AI074973, U54AI057160)
Topics: Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
Keywords: IRF3, IRF5, IRF7, type I interferon, myeloid dendritic cells, MAVS, interferon-stimulated genes, West Nile virus, murine norovirus, positive-strand RNA viruses, interferon-beta, Toll-like receptor signaling, RIG-I-like receptor signaling, transcription factors, macrophages, viral pathogenesis
MeSH terms: Animals, Dendritic Cells, Macrophages, Mice, Inbred C57BL, West Nile Fever, West Nile virus, Signal Transduction, Interferon-beta, Mice, Knockout, Viral Load, Myeloid Cells, Adaptor Proteins, Signal Transducing, Interferon Regulatory Factors, Interferon Regulatory Factor-3, Interferon Regulatory Factor-7, Toll-Like Receptors, Mice, Receptor, Interferon alpha-beta

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IRF-3, IRF-5, and IRF-7 Coordinately Regulate the Type I IFN Response in Myeloid Dendritic Cells Downstream of MAVS Signaling

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