Evidence map›Paper›PMID 29997111›Full record

ArticleAnnals of the rheumatic diseases2018

Glucocorticoid receptor in stromal cells is essential for glucocorticoid-mediated suppression of inflammation in arthritis.

Mascha Koenen, Stephan Culemann, Sabine Vettorazzi, Giorgio Caratti, Lucien Frappart, Wolfgang Baum, Gerhard Krönke, Ulrike Baschant, Jan P Tuckermann

Open access · bronzeAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 61 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Mascha KoenenInstitute for Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Stephan CulemannTuckermann Lab, Leibniz Institute for Age Research-Fritz-Lipmann-Institute, Jena, Germany.
Sabine VettorazziInstitute for Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Giorgio CarattiInstitute for Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Lucien FrappartTuckermann Lab, Leibniz Institute for Age Research-Fritz-Lipmann-Institute, Jena, Germany.
Wolfgang BaumDepartment of Internal Medicine 3 and Institute for Clinical Immunology, University Hospital Erlangen, Erlangen, Germany.
Gerhard KrönkeDepartment of Internal Medicine 3 and Institute for Clinical Immunology, University Hospital Erlangen, Erlangen, Germany.
Ulrike Baschant *Tuckermann Lab, Leibniz Institute for Age Research-Fritz-Lipmann-Institute, Jena, Germany.
Jan P Tuckermann *Institute for Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DEUniversitätsklinikum Erlangen · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlucocorticoid (GC) therapy is frequently used to treat rheumatoid arthritis due to potent anti-inflammatory actions of GCs. Direct actions of GCs on immune cells were suggested to suppress inflammation.

objectivesDefine the role of the glucocorticoid receptor (GR) in stromal cells for suppression of inflammatory arthritis.

methodsBone marrow chimeric mice lacking the GR in the hematopoietic or stromal compartment, respectively, and mice with impaired GR dimerisation (GR

resultsGR deficiency in immune cells did not impair GC-mediated suppression of STIA. In contrast, mice with GR-deficient or GR dimerisation-impaired stromal cells were resistant to GC treatment, despite efficient suppression of cytokines. Intriguingly, in mice with impaired GR function in the stromal compartment, GCs failed to stimulate non-classical, non-activated macrophages (Ly6C

conclusionWe report a novel anti-inflammatory mechanism of GC action that involves GR dimerisation-dependent gene regulation in non-immune stromal cells, presumably FLS. FLS control non-classical, anti-inflammatory polarisation of macrophages that contributes to suppression of inflammation in arthritis.

Indexed as

AnimalsAnti-Inflammatory AgentsArthritis, ExperimentalArthritis, RheumatoidCytokinesDexamethasoneDimerizationGene Expression RegulationGlucocorticoidsMetabolism, Inborn ErrorsMice, Inbred BALB CMice, Inbred C57BLReceptors, GlucocorticoidStromal CellsSynoviocytesTransplantation ChimeraAnti-Inflammatory AgentsCytokinesDexamethasoneGlucocorticoidsReceptors, Glucocorticoidarthritiscorticosteroidsfibroblastsinflammation

Identifiers

PMID29997111
PMCPMC6225806
OpenAlexW2850263944

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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.