Evidence map›Paper›PMID 31507614›Full record

ReviewFrontiers in immunology2019

More Than Suppression: Glucocorticoid Action on Monocytes and Macrophages.

Jan M Ehrchen, Johannes Roth, Katarzyna Barczyk-Kahlert

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
119citing papers in PubMed, 2 pooled it
8.4field-weighted citation impact, top 2% 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

119 citing papers in PubMed, 2 syntheses or guidelines pooled it, 188 citations in OpenAlex.

  1. Immunomodulatory interventions for focal epilepsy.The Cochrane database of systematic reviews · 2023
    Pooled it
  2. Pooled it
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  14. Observational
  15. Review
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  17. Synovial MS4A4A correlates with inflammation and counteracts response to corticosteroids in arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  18. Article
  19. IgE and non-IgE-mediated pathways in anaphylaxis.Seminars in immunopathology · 2025
    Review
  20. Review

59 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Jan M EhrchenDepartment of Dermatology, University of Münster, Münster, Germany.
Johannes RothInstitute of Immunology, University of Münster, Münster, Germany.
Katarzyna Barczyk-KahlertInstitute of Immunology, University of Münster, Münster, Germany.
University of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uncontrolled inflammation is a leading cause of many clinically relevant diseases. Current therapeutic strategies focus mainly on immunosuppression rather than on the mechanisms of inflammatory resolution. Glucocorticoids (GCs) are still the most widely used anti-inflammatory drugs. GCs affect most immune cells but there is growing evidence for cell type specific mechanisms. Different subtypes of monocytes and macrophages play a pivotal role both in generation as well as resolution of inflammation. Activation of these cells by microbial products or endogenous danger signals results in production of pro-inflammatory mediators and initiation of an inflammatory response. GCs efficiently inhibit these processes by down-regulating pro-inflammatory mediators from macrophages and monocytes. On the other hand, GCs act on "naïve" monocytes and macrophages and induce anti-inflammatory mediators and differentiation of anti-inflammatory phenotypes. GC-induced anti-inflammatory monocytes have an increased ability to migrate toward inflammatory stimuli. They remove endo- and exogenous danger signals by an increased phagocytic capacity, produce anti-inflammatory mediators and limit T-cell activation. Thus, GCs limit amplification of inflammation by repressing pro-inflammatory macrophage activation and additionally induce anti-inflammatory monocyte and macrophage populations actively promoting resolution of inflammation. Further investigation of these mechanisms should lead to the development of novel therapeutic strategies to modulate undesirable inflammation with fewer side effects via induction of inflammatory resolution rather than non-specific immunosuppression.

Indexed as

Antigen PresentationBiomarkersCell AdhesionDisease SusceptibilityGenetic Predisposition to DiseaseGlucocorticoidsHumansImmunity, InnateImmunomodulationImmunosuppressive AgentsInflammationInflammation MediatorsLymphocyte ActivationMacrophagesMonocytesPhagocytosisBiomarkersGlucocorticoidsImmunosuppressive AgentsInflammation Mediatorsanti-inflammatoryglucocorticoidsmacrophagemonocyteresolution of inflammation

Identifiers

PMID31507614
PMCPMC6718555
OpenAlexW2968206736

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.