Evidence map›Paper›PMID 30032131›Full record

ArticleJournal of innate immunity2018

The Anaphylatoxin C3a Receptor Expression on Human M2 Macrophages Is Down-Regulated by Stimulating the Histamine H4 Receptor and the IL-4 Receptor.

Susanne Mommert, Derya Aslan, Lisanne Ratz, Holger Stark, Ralf Gutzmer, Thomas Werfel

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. IgE and non-IgE-mediated pathways in anaphylaxis.Seminars in immunopathology · 2025
    Review
  4. Article
  5. Complement receptorBrain communications · 2025
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. The role of the histamine HBritish journal of pharmacology · 2020
    Review
  14. Article
  15. Review
  16. Tackling the Pros and Cons of Inflammation.Journal of innate immunity · 2019
    Article
  17. With Complement.Journal of innate immunity · 2018
    Article
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

6 authors at 2 institutions in 1 country.

Susanne MommertDivision of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Derya AslanDivision of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Lisanne RatzDivision of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Holger StarkInstitute of Pharmaceutical and Medicinal Chemistry, Heinrich Heine University, Duesseldorf, Germany.
Ralf GutzmerDivision of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Thomas WerfelDivision of Immunodermatology and Allergy Research, Department of Dermatology and Allergy, Hannover Medical School, Hannover, Germany.
Medizinische Hochschule Hannover · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The anaphylatoxin C3a triggers inflammation by binding to its specific G-protein-coupled C3a receptor (C3aR). Since the number of C3aR, which is expressed on the cell surface, affects the response to C3a, we investigated the expression levels of C3aR on human M2 macrophages in allergic situations where high levels of the Th2 cytokine IL-4 and histamine are present in a local microenvironment. The histamine H1 receptor (H1R), H2R and the H4R mRNA expressions were induced or up-regulated during the differentiation process of M2 macrophages. The presence of histamine or agonists targeting the H1R, H2R and, in particular, the H4R during in vitro differentiation from monocytes to macrophages modified the M2 phenotype by regulating the macrophage differentiation marker CD68 and CD163 expressions. In -addition, the C3aR expression was also down-regulated by -ST-1006 during this process. Histamine and ST-1006 down-regulated the expression of C3aR with different time kinetics on fully differentiated M2 macrophages. By analysing C3a-induced IL-6 mRNA expression, we observed a diminished response to C3a in ST-1006-treated M2 macrophages when compared to un-treated cells. Expression of C3 was not affected by histamine, whereas IL-4 strongly down-regulated C3aR and C3 expressions. Our data suggests that down-regulation of C3aR expression by mediators present in allergic situations such as IL-4 or histamine has an anti-inflammatory impact by reducing the sensitivity to C3a-induced down-stream signaling, thereby contributing to the regulation of local inflammatory responses in the skin.

Indexed as

Cell DifferentiationCells, CulturedComplement C3Down-RegulationHistamineHumansHypersensitivityInterleukin-4MacrophagesPiperazinesPyrimidinesReceptors, ComplementReceptors, Histamine H4Receptors, Interleukin-4SkinTh2 CellsC3 protein, humanComplement C3complement C3a receptorHistamineInterleukin-4N4-(2,6-dichlorobenzyl)-6-(4-methylpiperazin-1-yl)pyrimidine-2,4-diaminePiperazinesPyrimidinesReceptors, ComplementReceptors, Histamine H4Receptors, Interleukin-4C3a receptorHistamine H4 receptorM2 macrophages

Identifiers

PMID30032131
PMCPMC6757164
OpenAlexW2886492534

What OpenQuestion holds

Textmetadata
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.