Cited by 412interferon and immune responsesImmune Response and InflammationImmunotherapy and Immune Responses

The interferon regulatory factor, IRF5, is a central mediator of toll-like receptor 7 signaling

Open access
Schoenemeyer, Annett, Barnes, Betsy J., Mancl, Margo.E., Latz, Eicke, Goutagny, Nadege, Pitha, Paula M., Fitzgerald, Katherine A., Golenbock, Douglas T.·2005·Journal of Biological Chemistry

Abstract

Interferon regulatory factors (IRFs) are critical components of virus-induced immune activation and type I interferon regulation. IRF3 and IRF7 are activated in response to a variety of viruses or after engagement of Toll-like receptor (TLR) 3 and TLR4 by double-stranded RNA and lipopolysaccharide, respectively. The activation of IRF5, is much more restricted. Here we show that in contrast to IRF3 and IRF7, IRF5 is not a target of the TLR3 signaling pathway but is activated by TLR7 or TLR8 signaling. We also demonstrate that MyD88, interleukin 1 receptor-associated kinase 1, and tumor necrosis factor receptor-associated factor 6 are required for the activation of IRF5 and IRF7 in the TLR7 signaling pathway. Moreover, ectopic expression of IRF5 enabled type I interferon production in response to TLR7 signaling, whereas knockdown of IRF5 by small interfering RNA reduced type I interferon induction in response to the TLR7 ligand, R-848. IRF5 and IRF7, therefore, emerge from these studies as critical mediators of TLR7 signaling.

Integrity signals

Registry

Crossref · 10.1074/jbc.m412584200

Cites

72 of 72 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

We couldn’t retrieve this paper’s full text, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • The prominent therapeutic efficacy of unmodified mRNA is possibly due to activation of endosomal TLR7/8 and subsequently causes pro-inflammatory cytokine secretion via MyD88-dependent IRF-5 phosphorylation.

    “The prominent therapeutic efficacy of unmodified mRNA is possibly due to activation of endosomal toll-like receptor 7/8 (TLR7/8) and subsequently causes pro-inflammatory cytokine secretion via MyD88-dependent IRF-5 phosphorylation (41).”

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Schoenemeyer, A., Barnes, B. J., Mancl, M. E., Latz, E., Goutagny, N., Pitha, P. M., Fitzgerald, K. A., & Golenbock, D. T.
Affiliations
  • University of Massachusetts Chan Medical School (US)
  • Johns Hopkins University (US)
Corresponding author
  • Fitzgerald, Katherine A.
  • Golenbock, Douglas T.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2005-04
Volume
280
Issue
17
Pages
17005-17012
ISSN
0021-9258 (ISSN-L)
OpenAlex
W2040706148
Cited by
411
References
72
Citations by year
2026: 7 · 2025: 8 · 2024: 16 · 2023: 16 · 2022: 11 · 2021: 13 · 2020: 16 · 2019: 21 · 2018: 23 · 2017: 25 · 2016: 11 · 2015: 14 · 2014: 25 · 2013: 17 · 2012: 20
FWCI
11.11
Type
journal article
Language
en
Open access
Locations
  • Journal of Biological Chemistry (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • eScholarship@UMassChan (submittedVersion)
Funders
  • National Cancer Institute (R01A1/CA19737-19A1)
  • National Institute of General Medical Sciences (GM 54060)
  • National Institute of Allergy and Infectious Diseases (AI-52455, AI 49309, R01AI049309)
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
IRF5, IRF7, TLR7, TLR8, TLR7 signaling, type I interferon, MyD88, TRAF6, IRAK1, IRF3, interferon regulatory factors, R848, innate immunity
MeSH terms
Antigens, Differentiation, Biological Assay, Cell Line, DNA-Binding Proteins, Dose-Response Relationship, Drug, Glutathione Transferase, Humans, Interferon Type I, Ligands, Lipopolysaccharides, Membrane Glycoproteins, Models, Biological, Phosphorylation, Receptors, Cell Surface, Receptors, Immunologic, Recombinant Fusion Proteins, RNA, Double-Stranded, Time Factors, Transcription Factors, Transfection, Signal Transduction, Genes, Reporter, Electroporation, Microscopy, Confocal, Reverse Transcriptase Polymerase Chain Reaction, RNA Interference, RNA, Small Interfering, Adaptor Proteins, Signal Transducing, Interferon Regulatory Factors, Interferon Regulatory Factor-3, Interferon Regulatory Factor-7, Toll-Like Receptors, Toll-Like Receptor 3, Toll-Like Receptor 4, Toll-Like Receptor 7, Toll-Like Receptor 8, Myeloid Differentiation Factor 88

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review