Evidence map›Paper›PMID 21160051›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

The role of glycogen synthase kinase 3 in regulating IFN-β-mediated IL-10 production.

Huizhi Wang, Jonathan Brown, Carlos A Garcia, Yunan Tang, Manjunatha R Benakanakere, Terrance Greenway, Pascale Alard, Denis F Kinane, Michael Martin

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 75 citations in OpenAlex.

  1. Modulation of TNF-induced macrophage polarization by synovial fibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2014
    Trial
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  6. EMT and Inflammation: Crossroads in HCC.Journal of gastrointestinal cancer · 2023
    Review
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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

9 authors at 3 institutions in 1 country.

Huizhi WangDepartment of Microbiology and Immunology, University of Louisville School of Medicine, Louisville, KY 40202, USA.
Jonathan Brown
Carlos A Garcia
Yunan Tang
Manjunatha R Benakanakere
Terrance Greenway
Pascale Alard
Denis F Kinane
Michael Martin
University of Louisville · USUniversity of Pennsylvania · USMississippi State University · US

Funding

Role of GSK3 in host inflammationR01DE017680 · NIDCR · UNIVERSITY OF LOUISVILLE · PI SCOTT, DAVID A · 2007 to 2017
$3.3M
Role of JAKs in innate responses to P. gingivalisR01DE017921 · NIDCR · UNIVERSITY OF LOUISVILLE · PI LAMONT, RICHARD J · 2010 to 2019
$3.3M
NIDCR NIH HHS R01 DE017680NIDCR NIH HHS R01DE017680NIDCR NIH HHS R01 DE017921NIDCR NIH HHS R01DE017921
6 · The paper itself

Abstract

The ability of IFN-β to induce IL-10 production from innate immune cells is important for its anti-inflammatory properties and is believed to contribute to its therapeutic value in treating multiple sclerosis patients. In this study, we identified that IFN-β stimulates IL-10 production by activating the JAK1- and PI3K-signaling pathways. JAK1 activity was required for IFN-β to activate PI3K and Akt1 that resulted in repression of glycogen synthase kinase 3 (GSK3)-β activity. IFN-β-mediated suppression of GSK3-β promoted IL-10, because IL-10 production by IFN-β-stimulated dendritic cells (DC) expressing an active GSK3-β knockin was severely reduced, whereas pharmacological or genetic inhibition of GSK3-β augmented IL-10 production. IFN-β increased the phosphorylated levels of CREB and STAT3 but only CREB levels were affected by PI3K. Also, a knockdown in CREB, but not STAT3, affected the capacity of IFN-β to induce IL-10 from DC. IL-10 production by IFN-β-stimulated DC was shown to suppress IFN-γ and IL-17 production by myelin oligodendrocyte glycoprotein-specific CD4(+) T cells, and this IL-10-dependent anti-inflammatory effect was enhanced by directly targeting GSK3 in DC. These findings highlight how IFN-β induces IL-10 production and the importance that IL-10 plays in its anti-inflammatory properties, as well as identify a therapeutic target that could be used to increase the IL-10-dependent anti-inflammatory properties of IFN-β.

Indexed as

AnimalsCD4-Positive T-LymphocytesCells, CulturedDendritic CellsEnzyme ActivationEpitopes, T-LymphocyteGene Knock-In TechniquesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansInflammation MediatorsInterferon-betaInterferon-gammaInterleukin-10Interleukin-17Intracellular FluidEpitopes, T-LymphocyteGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIL10 protein, humanInflammation MediatorsInterferon-betaInterferon-gammaInterleukin-10Interleukin-17JAK1 protein, humanJanus Kinase 1MOG protein, humanMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsPhosphatidylinositol 3-Kinases

Identifiers

PMID21160051
PMCPMC3606930
OpenAlexW1501416341

What OpenQuestion holds

Textmetadata
LicenceTDM
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.