Evidence map›Paper›PMID 23853595›Full record

ArticlePLoS pathogens2013

Reprogramming of murine macrophages through TLR2 confers viral resistance via TRAF3-mediated, enhanced interferon production.

Darren J Perkins, Swamy K Polumuri, Meghan E Pennini, Wendy Lai, Ping Xie, Stefanie N Vogel

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Interferon-β regulates proresolving lipids to promote the resolution of acute airway inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Darren J PerkinsDepartment of Microbiology and Immunology, University of Maryland, Baltimore (UMB), School of Medicine, Baltimore, Maryland, United States of America.
Swamy K Polumuri
Meghan E Pennini
Wendy Lai
Ping Xie
Stefanie N Vogel
University of Maryland, Baltimore · USRutgers, The State University of New Jersey · US

Funding

DIFFERENTIATIVE SIGNALS FOR MACROPHAGE ACTIVATIONR37AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2000 to 2009
$5.3M
DIFFERENTIATIVE SIGNALS FOR MACROPHANGE ACTIVATIONR01AI018797 · NIAID · U.S. UNIFORMED SERVICES UNIV OF HLTH SCI · PI VOGEL, STEFANIE N. · 1985 to 2014
$3.8M
Differentiative Signals for Macrophage ActivationR56AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2015 to 2015
$506k
NIAID NIH HHS R01 AI018797NIAID NIH HHS R01 AI18797NIAID NIH HHS R37 AI018797NIAID NIH HHS R56 AI018797
6 · The paper itself

Abstract

The cell surface/endosomal Toll-like Receptors (TLRs) are instrumental in initiating immune responses to both bacteria and viruses. With the exception of TLR2, all TLRs and cytosolic RIG-I-like receptors (RLRs) with known virus-derived ligands induce type I interferons (IFNs) in macrophages or dendritic cells. Herein, we report that prior ligation of TLR2, an event previously shown to induce "homo" or "hetero" tolerance, strongly "primes" macrophages for increased Type I IFN production in response to subsequent TLR/RLR signaling. This occurs by increasing activation of the transcription factor, IFN Regulatory Factor-3 (IRF-3) that, in turn, leads to enhanced induction of IFN-β, while expression of other pro-inflammatory genes are suppressed (tolerized). In vitro or in vivo "priming" of murine macrophages with TLR2 ligands increase virus-mediated IFN induction and resistance to infection. This priming effect of TLR2 is mediated by the selective upregulation of the K63 ubiquitin ligase, TRAF3. Thus, we provide a mechanistic explanation for the observed antiviral actions of MyD88-dependent TLR2 and further define the role of TRAF3 in viral innate immunity.

Indexed as

Cellular ReprogrammingImmunity, InnateUp-RegulationAnimalsCell LineCells, CulturedFemaleHumansInfluenza A virusInterferon Type ILigandsMacrophages, PeritonealMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutInterferon Type ILigandsRecombinant ProteinsTlr2 protein, mouseTNF Receptor-Associated Factor 3Toll-Like Receptor 2

Identifiers

PMID23853595
PMCPMC3708851
OpenAlexW1977429554

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.