Evidence map›Paper›PMID 12782719›Full record

ArticleThe Journal of experimental medicine2003

Inhibition of interleukin 10 signaling after Fc receptor ligation and during rheumatoid arthritis.

Jong-Dae Ji, Ioannis Tassiulas, Kyung-Hyun Park-Min, Ani Aydin, Ingrid Mecklenbrauker, Alexander Tarakhovsky, Luminita Pricop, Jane E Salmon, Lionel B Ivashkiv

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 78 citations in OpenAlex.

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  19. Macrophages in synovial inflammation.Frontiers in immunology · 2011
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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.

Jong-Dae JiDepartment of Medicine Hospital for Special Surgery, 535 East 70th St., New York, NY 10021, USA.
Ioannis Tassiulas
Kyung-Hyun Park-Min
Ani Aydin
Ingrid Mecklenbrauker
Alexander Tarakhovsky
Luminita Pricop
Jane E Salmon
Lionel B Ivashkiv
Hospital for Special Surgery · USCornell University · USRockefeller University · US

Funding

Inhibition of STAT3 and inflammatory cytokine productionR01AI044938 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 2000 to 2025
$9.2M
CYTOKINE REGULATION OF RA SYNOVIOCYTE PHENOTYPER01AR046713 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 1999 to 2025
$8.3M
FCGAMMA RECEPTOR IN IMMUNE-COMPLEX MEDIATED INFLAMMATIONR03AR047106 · NIAMS · HOSPITAL FOR SPECIAL SURGERY · PI PRICOP, LUMINITA ANA · 2000 to 2002
$243k
INHIBITION OF IL-6 AND STAT3 IN RHEUMATOID ARTHRITISR21AI044938 · NIAID · HOSPITAL FOR SPECIAL SURGERY · PI IVASHKIV, LIONEL B · 1999 to 1999
–
NIAID NIH HHS AI44938NIAID NIH HHS R01 AI044938NIAID NIH HHS R21 AI044938NIAMS NIH HHS AR46713NIAMS NIH HHS AR47106NIAMS NIH HHS R01 AR046713
6 · The paper itself

Abstract

Interleukin-10 (IL-10) is a potent deactivator of myeloid cells that limits the intensity and duration of immune and inflammatory responses. The activity of IL-10 can be suppressed during inflammation, infection, or after allogeneic tissue transplantation. We investigated whether inflammatory factors suppress IL-10 activity at the level of signal transduction. Out of many factors tested, only ligation of Fc receptors by immune complexes inhibited IL-10 activation of the Jak-Stat signaling pathway. IL-10 signaling was suppressed in rheumatoid arthritis joint macrophages that are exposed to immune complexes in vivo. Activation of macrophages with interferon-gamma was required for Fc receptor-mediated suppression of IL-10 signaling, which resulted in diminished activation of IL-10-inducible genes and reversal of IL-10-dependent suppression of cytokine production. The mechanism of inhibition involved decreased cell surface IL-10 receptor expression and Jak1 activation and was dependent on protein kinase C delta. These results establish that IL-10 signaling is regulated during inflammation and identify Fc receptors and interferon-gamma as important regulators of IL-10 activity. Generation of macrophages refractory to IL-10 can contribute to pathogenesis of inflammatory and infectious diseases characterized by production of interferon-gamma and immune complexes.

Indexed as

Antigen-Antibody ComplexArthritis, RheumatoidBase SequenceDNAHumansInterferon-gammaInterleukin-10In Vitro TechniquesMacrophage ActivationMacrophagesProtein Kinase CReceptors, IgGSignal TransductionAntigen-Antibody ComplexDNAInterferon-gammaInterleukin-10Protein Kinase CReceptors, IgG

Identifiers

PMID12782719
PMCPMC2193912
OpenAlexW2170237342

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.