Evidence map›Paper›PMID 25170774›Full record

ArticlePloS one2014

Bruton's tyrosine kinase and protein kinase C µ are required for TLR7/9-induced IKKα and IRF-1 activation and interferon-β production in conventional dendritic cells.

Yan-Feng Li, Koon-Guan Lee, Xijun Ou, Kong-Peng Lam

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  5. Unexpected CD5Journal of clinical medicine · 2023
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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

4 authors at 2 institutions in 1 country.

Yan-Feng LiImmunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore, Singapore.
Koon-Guan LeeImmunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore, Singapore.
Xijun OuImmunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore, Singapore.
Kong-Peng LamImmunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore, Singapore; Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore; Department of Pediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Agency for Science, Technology and Research · SGBioprocessing Technology Institute · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stimulation of TLR7/9 by their respective ligands leads to the activation of IκB kinase α (IKKα) and Interferon Regulatory Factor 1 (IRF-1) and results in interferon (IFN)-β production in conventional dendritic cells (cDC). However, which other signaling molecules are involved in IKKα and IRF-1 activation during TLR7/9 signaling pathway are not known. We and others have shown that Bruton's Tyrosine Kinase (BTK) played a part in TLR9-mediated cytokine production in B cells and macrophages. However, it is unclear if BTK participates in TLR7/9-induced IFN-β production in cDC. In this study, we show that BTK is required for IFN-β synthesis in cDC upon TLR7/9 stimulation and that stimulated BTK-deficient cDC are defective in the induction of IKKα/β phosphorylation and IRF-1 activation. In addition, we demonstrate that Protein Kinase C µ (PKCµ) is also required for TLR7/9-induced IRF-1 activation and IFN-β upregulation in cDC and acts downstream of BTK. Taken together, we have uncovered two new molecules, BTK and PKCµ, that are involved in TLR7/9-triggered IFN-β production in cDC.

Indexed as

Agammaglobulinaemia Tyrosine KinaseAnimalsDendritic CellsGene DeletionI-kappa B KinaseInterferon-betaInterferon Regulatory Factor-1Mice, Inbred C57BLProtein Kinase CProtein-Tyrosine KinasesToll-Like Receptor 7Toll-Like Receptor 9Agammaglobulinaemia Tyrosine KinaseBtk protein, mouseI-kappa B KinaseInterferon-betaInterferon Regulatory Factor-1Protein Kinase Cprotein kinase DProtein-Tyrosine KinasesToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID25170774
PMCPMC4149510
OpenAlexW2090432164

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.