Evidence map›Paper›PMID 25412261›Full record

ArticlePLoS neglected tropical diseases2014

Antibody-dependent enhancement infection facilitates dengue virus-regulated signaling of IL-10 production in monocytes.

Tsung-Ting Tsai, Yi-Jui Chuang, Yee-Shin Lin, Chih-Peng Chang, Shu-Wen Wan, Sheng-Hsiang Lin, Chia-Ling Chen, Chiou-Feng Lin

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Dengue and COVID-19: two sides of the same coin.Journal of biomedical science · 2022
    Review
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  15. Observational
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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

8 authors at 2 institutions in 1 country.

Tsung-Ting TsaiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yi-Jui ChuangDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yee-Shin LinInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Center of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan.
Chih-Peng ChangInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Department of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Shu-Wen WanCenter of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan.
Sheng-Hsiang LinInstitute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Chia-Ling ChenCenter of Translational Medicine, Taipei Medical University, Taipei, Taiwan.
Chiou-Feng LinCenter of Infectious Disease and Signaling Research, National Cheng Kung University, Tainan, Taiwan; Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan; Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Microbiology and Immunology, College of Medicine, Taipei Medical University, Taipei, Taiwan.
National Cheng Kung University · TWTaipei Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterleukin (IL)-10 levels are increased in dengue virus (DENV)-infected patients with severe disorders. A hypothetical intrinsic pathway has been proposed for the IL-10 response during antibody-dependent enhancement (ADE) of DENV infection; however, the mechanisms of IL-10 regulation remain unclear. PRINCIPLE FINDING: We found that DENV infection and/or attachment was sufficient to induce increased expression of IL-10 and its downstream regulator suppressor of cytokine signaling 3 in human monocytic THP-1 cells and human peripheral blood monocytes. IL-10 production was controlled by activation of cyclic adenosine monophosphate response element-binding (CREB), primarily through protein kinase A (PKA)- and phosphoinositide 3-kinase (PI3K)/PKB-regulated pathways, with PKA activation acting upstream of PI3K/PKB. DENV infection also caused glycogen synthase kinase (GSK)-3β inactivation in a PKA/PI3K/PKB-regulated manner, and inhibition of GSK-3β significantly increased DENV-induced IL-10 production following CREB activation. Pharmacological inhibition of spleen tyrosine kinase (Syk) activity significantly decreased DENV-induced IL-10 production, whereas silencing Syk-associated C-type lectin domain family 5 member A caused a partial inhibition. ADE of DENV infection greatly increased IL-10 expression by enhancing Syk-regulated PI3K/PKB/GSK-3β/CREB signaling. We also found that viral load, but not serotype, affected the IL-10 response. Finally, modulation of IL-10 expression could affect DENV replication. SIGNIFICANCE: These results demonstrate that, in monocytes, IL-10 production is regulated by ADE through both an extrinsic and an intrinsic pathway, all involving a Syk-regulated PI3K/PKB/GSK-3β/CREB pathway, and both of which impact viral replication.

Indexed as

Antibody-Dependent EnhancementCell LineDengueDengue VirusHost-Pathogen InteractionsHumansInterleukin-10MonocytesSignal TransductionVirus ReplicationIL10 protein, humanInterleukin-10

Identifiers

PMID25412261
PMCPMC4239119
OpenAlexW1980143030

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.