Evidence map›Paper›PMID 31253169›Full record

ArticleArthritis research & therapy2019

Prostaglandin receptor EP4 expression by Th17 cells is associated with high disease activity in ankylosing spondylitis.

Charlotte Klasen, Anja Meyer, Paula S Wittekind, Iris Waqué, Schafiq Nabhani, David M Kofler

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Environmental and Genetic Determinants of Ankylosing Spondylitis.International journal of molecular sciences · 2024
    Review
  8. Case of MOG-IgG-associated disease with ankylosing spondylitis: A rare coexistence.Turkish journal of physical medicine and rehabilitation · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Uncovering the Underworld of Axial Spondyloarthritis.International journal of molecular sciences · 2023
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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 1 institution in 1 country.

Charlotte KlasenDivision of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, Kerpenerstr. 62, 50937, Cologne, Germany.
Anja MeyerDivision of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, Kerpenerstr. 62, 50937, Cologne, Germany.
Paula S WittekindDivision of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, Kerpenerstr. 62, 50937, Cologne, Germany.
Iris WaquéDivision of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, Kerpenerstr. 62, 50937, Cologne, Germany.
Schafiq NabhaniDivision of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, Kerpenerstr. 62, 50937, Cologne, Germany.
David M KoflerDivision of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, Kerpenerstr. 62, 50937, Cologne, Germany. david.kofler@uk-koeln.de.ORCID 0000-0001-6164-3980
University of Cologne · DE

Funding

Fritz Thyssen Stiftung 10.17.2.019MNUniversität zu Köln Köln Fortune Program
6 · The paper itself

Abstract

backgroundTh17 cells are involved in the pathogenesis of ankylosing spondylitis (AS). However, the mechanism underlying enhanced Th17 cell accumulation in AS remains unknown. The prostaglandin E

methodsTh17 cells from patients with AS were analyzed for the transcriptional expression of prostaglandin receptor genes by quantitative RT-PCR. Th17 cells from patients with rheumatoid arthritis (RA) and from healthy individuals served as controls. EP4 receptor expression in Th17 cells was assessed ex vivo by flow cytometry and by western blot. Functional analysis using EP4-specific agonists was performed to reveal how EP4 regulates Th17 cells.

resultsEP4 is significantly overexpressed in Th17 cells from patients with AS compared to Th17 cells from healthy individuals or patients with RA or psoriatic arthritis (PsA). EP4 upregulation is unique to Th17 cells and is not found in other CD4

conclusionsEP4 is a potential marker of disease activity in patients with AS. Aberrant EP4 expression might contribute to pathogenic Th17 cell accumulation and represent a new target for the treatment of AS.

Indexed as

Gene Expression RegulationAdultAllelesBiomarkersBlotting, WesternCell DifferentiationCells, CulturedFemaleGenome-Wide Association StudyHumansMaleMiddle AgedReceptors, Prostaglandin E, EP4 SubtypeRNASignal TransductionSpondylitis, AnkylosingBiomarkersPTGER4 protein, humanReceptors, Prostaglandin E, EP4 SubtypeRNAAnkylosing spondylitisFoxO1Interleukin-23 receptorProstaglandin receptor EP4PTGER4Rheumatoid arthritisTh17 cells

Identifiers

PMID31253169
PMCPMC6599260
OpenAlexW2953707806

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.