Evidence map›Paper›PMID 20621581›Full record

ArticleBrain, behavior, and immunity2010

Epinephrine-primed murine bone marrow-derived dendritic cells facilitate production of IL-17A and IL-4 but not IFN-γ by CD4+ T cells.

Byung-Jin Kim, Harlan P Jones

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. A molecular systems architecture of asthma.Frontiers in immunology · 2026
    Pooled it
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  15. Driving βFrontiers in immunology · 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

2 authors at 2 institutions in 1 country.

Byung-Jin KimDepartment of Molecular Biology and Immunology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA.
Harlan P Jones
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

Visceral Fat & Lipid & Inflammatory Risk factors: Role of EthnicityP20MD001633 · NIMHD · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI CAFFREY, JAMES · 2005 to 2009
$7.1M
NIMHD NIH HHS L60 MD002372NIMHD NIH HHS P20 MD001633
6 · The paper itself

Abstract

Sympathetic activation leading to the release of epinephrine and norepinephrine, is known as an important regulatory circuit related to immune-mediated diseases. However, questions still remain on the behavior of antigen presenting cells (APC) dictated by stress-induced sympathetic neurotransmitters. The purpose of this study was to examine the fate of bone marrow-derived dendritic cell (BMDC)-associated influences on resting CD4(+) T cell activation. We hypothesize that pre-exposure of dendritic cells (DCs) can modify the intensity of cytokine production, leading to preference in resting CD4(+) T cell activation. BMDCs were pre-treated with epinephrine for 2h followed by subsequent treatment of lipopolysaccharide (LPS). Subsequently, BMDCs were cocultured with purified CD4(+) T cells from mouse spleen in the absence or presence of anti-CD3 stimulation in epinephrine-free media. Epinephrine pre-treatment enhanced surface expression of MHCII, CD80 and CD86. Quantitative RT-PCR showed that epinephrine pre-treatment induced a significant transcriptional decrease of IL-12p40 and a significant increase of IL-12p35 and IL-23p19. In addition, β2-adrenergic-blockade was shown to reverse these effects. Epinephrine pre-treatment also induced a significant decrease of IL-12p70 and a significant increase of IL-23 and IL-10 cytokine production. Importantly, these changes corresponded with increased IL-4 and IL-17A, but not IFN-g cytokine production by CD4(+) T cells in a b2-adrenergic receptor-dependent manner. These results suggest that exposure to stress-derived epinephrine dictates dendritic cells to generate a dominant Th2/Th17 phenotype in the context of subsequent exposure to a pathogenic stimulus.

Indexed as

Adrenergic beta-2 Receptor AntagonistsAdrenergic beta-AgonistsAnimalsAntibodies, MonoclonalB7-1 AntigenB7-2 AntigenBone Marrow CellsCD3 ComplexCD4-Positive T-LymphocytesCells, CulturedDendritic CellsEnzyme-Linked Immunosorbent AssayEpinephrineFlow CytometryGenes, MHC Class IIInterferon-gammaAdrenergic beta-2 Receptor AntagonistsAdrenergic beta-AgonistsAntibodies, MonoclonalB7-1 AntigenB7-2 AntigenCD3 ComplexEpinephrineInterferon-gammaInterleukin-10Interleukin-12Interleukin-12 Subunit p35Interleukin-12 Subunit p40Interleukin-17Interleukin-23Interleukin-23 Subunit p19Interleukin-4Lipopolysaccharides

Identifiers

PMID20621581
PMCPMC2939238
OpenAlexW2030825630

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.