Evidence map›Paper›PMID 17059692›Full record

ArticleJournal of endotoxin research2006

Transcriptional regulation of lipopolysaccharide (LPS)-induced Toll-like receptor (TLR) expression in murine macrophages: role of interferon regulatory factors 1 (IRF-1) and 2 (IRF-2).

Quan M Nhu, Natalia Cuesta, Stefanie N Vogel

Abstract read
In one paragraph

Article in Journal of endotoxin research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

32 citing papers in PubMed, 57 citations in OpenAlex.

  1. Trial
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  4. Article
  5. International journal of molecular sciences · 2022
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  6. Article
  7. Review
  8. Article
  9. Article
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  11. Article
  12. HCFC2 is needed for IRF1- and IRF2-dependentThe Journal of experimental medicine · 2017
    Article
  13. Regulation of microglial activation in stroke.Acta pharmacologica Sinica · 2017
    Review
  14. Article
  15. Article
  16. Study on the Inhibitory Effects of Ephedra AconiteEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  17. Article
  18. Article
  19. Article
  20. Exogenous heat shock protein HSP70 modulates lipopolysaccharide-induced macrophage activation.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2013
    Article
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

3 authors at 1 institution in 1 country.

Quan M NhuDepartment of Microbiology and Immunology, University of Maryland Baltimore (UMB), School of Medicine, Baltimore, MD 21201, USA.
Natalia Cuesta
Stefanie N Vogel
University of Maryland, Baltimore · 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
IMMUNITY AND INFECTIONT32AI007540 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI KAPER, JAMES B · 1998 to 2018
$2.2M
Differentiative Signals for Macrophage ActivationR56AI018797 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI VOGEL, STEFANIE N. · 2015 to 2015
$506k
NIAID NIH HHS AI-07540NIAID NIH HHS AI-18797NIAID NIH HHS R01 AI018797NIAID NIH HHS R37 AI018797NIAID NIH HHS R56 AI018797NIAID NIH HHS T32 AI007540
6 · The paper itself

Abstract

Activation of TLRs is most closely associated with induction of pro-inflammatory gene expression; however, expression of many other genes, including the TLR genes themselves, has also been shown to be modulated following TLR engagement. A large family of nuclear transcription factors, the interferon regulatory factors (IRFs), have been implicated in TLR signaling leading to pro-inflammatory gene expression. Given that IRF-1 and IRF-2 counter-regulate the transcriptional activity of many genes, we hypothesized that IRF-1 and IRF-2 might also regulate TLR gene expression following LPS stimulation of murine macrophages. mRNA derived from medium- or LPS-treated primary peritoneal macrophages was analyzed for TLR gene expression using quantitative real-time PCR. In wild-type macrophages, LPS up-regulated expression of TLRs 1-3 and 6-9 steady-state mRNA, while TLR4 mRNA was modestly down-regulated. IRF-2(-/-) macrophages responded to LPS with dysregulated expression of TLR3, TLR4, and TLR5 mRNA, whereas IRF-1 deficiency dampened LPS-induced mRNA expression for TLR3, TLR6, and TLR9. Functional studies revealed aberrant TLR3 signaling in IRF-2(-/-) macrophages. Collectively, these findings reveal an additional level of complexity associated with TLR transcriptional regulation and suggest that the trans-acting factors, IRF-1 and IRF-2, contribute to the innate immune response to infections by regulating TLR gene expression.

Indexed as

Transcription, GeneticAnimalsCells, CulturedGene Expression RegulationInterferon Regulatory Factor-1Interferon Regulatory Factor-2LipopolysaccharidesMacrophages, PeritonealMiceMice, Inbred C57BLRNA, MessengerToll-Like ReceptorsInterferon Regulatory Factor-1Interferon Regulatory Factor-2LipopolysaccharidesRNA, MessengerToll-Like Receptors

Identifiers

PMID17059692
PMCPMC5930016
OpenAlexW2008699975

What OpenQuestion holds

Textmetadata
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.