Evidence map›Paper›PMID 37287978›Full record

ArticleFrontiers in immunology2023

Transcriptomic signatures reveal a shift towards an anti-inflammatory gene expression profile but also the induction of type I and type II interferon signaling networks through aryl hydrocarbon receptor activation in murine macrophages.

Johannes R Schmidt, Janine Haupt, Sina Riemschneider, Christoph Kämpf, Dennis Löffler, Conny Blumert, Kristin Reiche, Ulrike Koehl, Stefan Kalkhof, Jörg Lehmann

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

4 citing papers in PubMed, 11 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

10 authors at 4 institutions in 1 country.

Johannes R SchmidtDepartment of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Janine HauptDepartment of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Sina RiemschneiderDepartment of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Christoph KämpfDepartment of Diagnostics, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Dennis LöfflerFraunhofer Cluster of Excellence Immune-Mediated Diseases (CIMD), Leipzig, Germany.
Conny BlumertFraunhofer Cluster of Excellence Immune-Mediated Diseases (CIMD), Leipzig, Germany.
Kristin ReicheDepartment of Diagnostics, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Ulrike KoehlFraunhofer Cluster of Excellence Immune-Mediated Diseases (CIMD), Leipzig, Germany.
Stefan KalkhofDepartment of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Jörg LehmannDepartment of Preclinical Development and Validation, Fraunhofer Institute for Cell Therapy and Immunology, Leipzig, Germany.
Fraunhofer Institute for Cell Therapy and Immunology · DEFraunhofer Research Institution for Materials Recycling and Resource Strategies IWKS · DECoburg University of Applied Sciences · DELeipzig University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates a broad range of target genes involved in the xenobiotic response, cell cycle control and circadian rhythm. AhR is constitutively expressed in macrophages (Mϕ), acting as key regulator of cytokine production. While proinflammatory cytokines, i.e., IL-1β, IL-6, IL-12, are suppressed through AhR activation, anti-inflammatory IL-10 is induced. However, the underlying mechanisms of those effects and the importance of the specific ligand structure are not yet completely understood. Methods: Therefore, we have compared the global gene expression pattern in activated murine bone marrow-derived macrophages (BMMs) subsequently to exposure with either benzo[ Results and discussion: In total, more than 1,000 differentially expressed genes (DEGs) could be mapped, covering a plethora of AhR-modulated effects on basal cellular processes, i.e., transcription and translation, but also immune functions, i.e., antigen presentation, cytokine production, and phagocytosis. Among DEGs were genes that are already known to be regulated by AhR, i.e.,

Indexed as

Interferon-gammaTranscriptomeAnimalsAnti-Inflammatory AgentsBasic Helix-Loop-Helix ProteinsCytokinesLigandsMacrophagesMiceReceptors, Aryl HydrocarbonAhr protein, mouseAnti-Inflammatory AgentsBasic Helix-Loop-Helix ProteinsCytokinesInterferon-gammaLigandsReceptors, Aryl Hydrocarbonaryl hydrocarbon receptorbenzo[a]pyreneimmunomodulationindol-3-carbinolinnate immunitymacrophage activationtranscriptomicstype I/II interferons

Identifiers

PMID37287978
PMCPMC10242070
OpenAlexW4378086096

What OpenQuestion holds

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LicenceCC BY
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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.