Evidence map›Paper›PMID 24129891›Full record

ArticleScientific reports2013

IL-32-PAR2 axis is an innate immunity sensor providing alternative signaling for LPS-TRIF axis.

Masanori Nakayama, Yasuo Niki, Toshiki Kawasaki, Yuki Takeda, Hiroyasu Ikegami, Yoshiaki Toyama, Takeshi Miyamoto

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-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

33 citing papers in PubMed, 72 citations in OpenAlex.

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  18. OncoTargets and therapy · 2021
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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

7 authors at 3 institutions in 1 country.

Masanori NakayamaDepartment of Orthopaedic Surgery, Keio University, 35 Shinanomachi, Shinjuku, Tokyo 160-8582, Japan.
Yasuo Niki
Toshiki Kawasaki
Yuki Takeda
Hiroyasu Ikegami
Yoshiaki Toyama
Takeshi Miyamoto
Keio University · JPKeio University Hospital · JPToho University Ohashi Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-32 is known to exert adujvant effects on innate immune response, however, receptors and downstream signaling pathways remain to be clarified. Here we found that IL-32γ upregulated serine protease activity of proteinase-3 (PR3), in turn triggering protease-activated receptor 2 (PAR2) signaling. Interestingly, silencing of PR3 or PAR2 using siRNA markedly diminished IL-32γ-induced TNFα and IFN-β mRNA expression. IL-32γ-PAR2 axis utilized TRIF and Ras-Raf-1 pathways. On stimulation with lipopolysaccharide (LPS), differential activation of protein kinase C isoforms modulated the balance between LPS-TLR4-TRIF and IL-32-PAR2-TRIF axes, because LPS was a strong inducer of IL-32γ. IL-32-PAR2-TRIF axis might serve not only as an extracellular sensor of bacterial and autologous proteases, but also as a modulator of innate and adaptive immunity during infection.

Indexed as

Signal TransductionAdaptor Proteins, Vesicular TransportGene Expression RegulationHumansImmunity, InnateInterferon-betaInterleukinsLipopolysaccharidesModels, BiologicalProtein Kinase CProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)Receptor, PAR-2Toll-Like ReceptorsTumor Necrosis Factor-alphaAdaptor Proteins, Vesicular TransportIL32 protein, humanInterferon-betaInterleukinsLipopolysaccharidesProtein Kinase CProto-Oncogene Proteins c-rafProto-Oncogene Proteins p21(ras)Receptor, PAR-2TICAM1 protein, humanToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID24129891
PMCPMC3797434
OpenAlexW2043928284

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.