Evidence map›Paper›PMID 24690905›Full record

ArticlePloS one2014

The role of interleukin-1 receptor-associated kinases in Vogt-Koyanagi-Harada disease.

Min Sun, Peizeng Yang, Liping Du, Yan Yang, Jian Ye

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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Min SunDepartment of Ophthalmology, Research Institute of Surgery & Daping Hospital, Third Military Medical University, Chongqing, P.R. China; The First Affiliated Hospital, Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, P. R. China.
Peizeng YangThe First Affiliated Hospital, Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, P. R. China.
Liping DuThe First Affiliated Hospital, Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, P. R. China.
Yan YangThe First Affiliated Hospital, Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing Eye Institute, Chongqing, P. R. China.
Jian YeDepartment of Ophthalmology, Research Institute of Surgery & Daping Hospital, Third Military Medical University, Chongqing, P.R. China.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CNDaping Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo explore whether IRAK1 and IRAK4 are involved in the pathogenesis of Vogt-Koyanagi-Harada (VKH) disease.

methodsThirty-nine VKH patients and thirty-two healthy controls were included in this study. The mRNA levels of IRAK1 and IRAK4 from active VKH patients, inactive VKH patients, and normal controls in peripheral blood mononuclear cells (PBMCs) were detected using real-time quantitative PCR. CD4(+)T cells were purified from PBMCs obtained from active VKH patients and normal controls. The effect of IRAK1/4 inhibition on CD4(+)T cell proliferation following stimulation with IL-18 or IL-1β was measured using a modified MTT assay. CD4(+)T cell expression of IFN-γ and IL-17 were detected by flow cytometry (FCM) and enzyme-linked immunosorbent assay (ELISA). The effect of IRAK1/4 inhibition on NF-κB, STAT1, and STAT3 activation was detected by FCM.

resultsThe mRNA levels of IRAK1 and IRAK4 were both significantly increased in active VKH patients compared to inactive VKH patients and healthy controls. No difference in the IRAK1 or IRAK4 mRNA level could be detected between inactive patients and healthy controls. After incubation with IRAK1/4 inhibitor, the proliferation of CD4(+)T cells was inhibited both in the active VKH patients and in the healthy controls. IRAK1/4 inhibition was also associated with a decreased expression of IFN-γ and IL-17. Phosphorylation of NF-κB, STAT1, and STAT3 in CD4(+)T from healthy controls was significantly decreased after inhibition of IRAK1/4.

conclusionsHigh mRNA levels of IRAK1 and IRAK4 correlated with VKH disease activity. IRAK1 and IRAK4 play a role in the activation and proliferation of CD4(+)T cells and the higher expression observed in VKH may contribute to the pathogenesis of this blinding condition.

Indexed as

AdultAntibodies, MonoclonalCase-Control StudiesCD4 Lymphocyte CountCD4-Positive T-LymphocytesFemaleGene ExpressionHumansInterferon-gammaInterleukin-17Interleukin-1 Receptor-Associated KinasesLeukocytes, MononuclearLymphocyte ActivationMaleMiddle AgedNF-kappa BAntibodies, MonoclonalInterferon-gammaInterleukin-17Interleukin-1 Receptor-Associated KinasesIRAK4 protein, humanNF-kappa BRNA, MessengerSTAT1 Transcription FactorSTAT3 Transcription Factor

Identifiers

PMID24690905
PMCPMC3972217
OpenAlexW2010339779

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.