Evidence map›Paper›PMID 35082159›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2022

TPL-2 Inhibits IFN-β Expression via an ERK1/2-TCF-FOS Axis in TLR4-Stimulated Macrophages.

Louise Blair, Michael J Pattison, Probir Chakravarty, Stamatia Papoutsopoulou, Latifa Bakiri, Erwin F Wagner, Stephen Smale, Steven C Ley

Open access · hybridAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. EBV Triggers a Distinct Antiviral Response in HMC3 Cells.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Role of TLRs as signaling cascades to combat infectious diseases: a review.Cellular and molecular life sciences : CMLS · 2025
    Review
  5. Article
  6. TPL2 kinase activity is required forFrontiers in immunology · 2025
    Article
  7. Article
  8. Article
  9. ERK1/2 in immune signalling.Biochemical Society transactions · 2022
    Review
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

8 authors at 3 institutions in 3 countries.

Louise BlairImmune Cell Signalling Laboratory, The Francis Crick Institute, London, United Kingdom.
Michael J PattisonImmune Cell Signalling Laboratory, The Francis Crick Institute, London, United Kingdom.
Probir ChakravartyBioinformatics and Biostatistics Technology Platform, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0003-1146-8824
Stamatia PapoutsopoulouImmune Cell Signalling Laboratory, The Francis Crick Institute, London, United Kingdom.ORCID 0000-0001-6665-8508
Latifa BakiriLaboratory of Genes and Disease, Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.ORCID 0000-0002-6300-2420
Erwin F WagnerLaboratory of Genes and Disease, Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Stephen SmaleDepartment of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA; and.
Steven C LeyImmune Cell Signalling Laboratory, The Francis Crick Institute, London, United Kingdom; steven.ley@ucl.ac.uk.ORCID 0000-0001-5911-9223
The Francis Crick Institute · GBMedical University of Vienna · ATUniversity of California, Los Angeles · US

Funding

Cancer Research UK FC001103Medical Research Council FC001103Medical Research Council MR/M016358/1Wellcome Trust FC001103
6 · The paper itself

Abstract

TPL-2 kinase plays an important role in innate immunity, activating ERK1/2 MAPKs in myeloid cells following TLR stimulation. We investigated how TPL-2 controls transcription in TLR4-stimulated mouse macrophages. TPL-2 activation of ERK1/2 regulated expression of genes encoding transcription factors, cytokines, chemokines, and signaling regulators. Bioinformatics analysis of gene clusters most rapidly induced by TPL-2 suggested that their transcription was mediated by the ternary complex factor (TCF) and FOS transcription factor families. Consistently, TPL-2 induced ERK1/2 phosphorylation of the ELK1 TCF and the expression of TCF target genes. Furthermore, transcriptomic analysis of TCF-deficient macrophages demonstrated that TCFs mediate approximately half of the transcriptional output of TPL-2 signaling, partially via induced expression of secondary transcription factors. TPL-2 signaling and TCFs were required for maximal TLR4-induced FOS expression. Comparative analysis of the transcriptome of TLR4-stimulated

Indexed as

Signal TransductionAnimalsGene Expression RegulationInterferon-betaLipopolysaccharidesMacrophage ActivationMacrophagesMAP Kinase Kinase KinasesMiceMice, KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene ProteinsProto-Oncogene Proteins c-fosTCF Transcription FactorsToll-Like Receptor 4Fos protein, mouseInterferon-betaLipopolysaccharidesMap3k8 protein, mouseMapk1 protein, mouseMapk3 protein, mouseMAP Kinase Kinase KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Proto-Oncogene ProteinsProto-Oncogene Proteins c-fosTCF Transcription FactorsToll-Like Receptor 4

Identifiers

PMID35082159
PMCPMC9012084
OpenAlexW4210820569

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.