Evidence map›Paper›PMID 22544928›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Prostaglandin E2 affects T cell responses through modulation of CD46 expression.

Karoline Kickler, Kathryn Maltby, Siobhán Ni Choileain, Jillian Stephen, Sheila Wright, David A Hafler, Henry N Jabbour, Anne L Astier

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

15 citing papers in PubMed, 31 citations in OpenAlex.

  1. Trial
  2. Review
  3. A CD4Immunity · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Complement as a regulator of adaptive immunity.Seminars in immunopathology · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. 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

8 authors at 4 institutions in 2 countries.

Karoline KicklerCentre for Inflammation Research, University of Edinburgh, Queen's Medical Research Institute, Edinburgh EH16 4TJ, United Kingdom.
Kathryn Maltby
Siobhán Ni Choileain
Jillian Stephen
Sheila Wright
David A Hafler
Henry N Jabbour
Anne L Astier
Queen's Medical Centre · GBMedical Research Council · GBCentre for Inflammation Research · GBYale University · US

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI David A. Hafler · 1996 to 2026
$51.7M
The function of T Bet in EAEP01NS038037 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2000 to 2010
$12.8M
T Cell Recognition of Myelin in Multiple SclerosisR37NS024247 · NINDS · YALE UNIVERSITY · PI HAFLER, DAVID A. · 2004 to 2010
$2.8M
Medical Research Council G0901697NIAID NIH HHS P01 AI039671NINDS NIH HHS P01 NS038037NINDS NIH HHS R37 NS024247
6 · The paper itself

Abstract

The ubiquitous protein CD46, a regulator of complement activity, promotes T cell activation and differentiation toward a regulatory Tr1-like phenotype. The CD46-mediated differentiation pathway is defective in several chronic inflammatory diseases, underlying the importance of CD46 in controlling T cell function and the need to understand its regulatory mechanisms. Using an RNA interference-based screening approach in primary T cells, we have identified that two members of the G protein-coupled receptor kinases were involved in regulating CD46 expression at the surface of activated cells. We have investigated the role of PGE(2), which binds to the E-prostanoid family of G protein-coupled receptors through four subtypes of receptors called EP 1-4, in the regulation of CD46 expression and function. Conflicting roles of PGE(2) in T cell functions have been reported, and the reasons for these apparent discrepancies are not well understood. We show that addition of PGE(2) strongly downregulates CD46 expression in activated T cells. Moreover, PGE(2) differentially affects T cell activation, cytokine production, and phenotype depending on the activation signals received by the T cells. This was correlated with a distinct pattern of the PGE(2) receptors expressed, with EP4 being preferentially induced by CD46 activation. Indeed, addition of an EP4 antagonist could reverse the effects observed on cytokine production after CD46 costimulation. These data demonstrate a novel role of the PGE(2)-EP4 axis in CD46 functions, which might at least partly explain the diverse roles of PGE(2) in T cell functions.

Indexed as

Cell ProliferationCells, CulturedDinoprostoneGene Expression RegulationG-Protein-Coupled Receptor Kinase 1HumansLymphocyte ActivationMembrane Cofactor ProteinReceptors, Prostaglandin E, EP2 SubtypeReceptors, Prostaglandin E, EP4 SubtypeRNA InterferenceT-Lymphocyte SubsetsCD46 protein, humanDinoprostoneG-Protein-Coupled Receptor Kinase 1GRK1 protein, humanMembrane Cofactor ProteinReceptors, Prostaglandin E, EP2 SubtypeReceptors, Prostaglandin E, EP4 Subtype

Identifiers

PMID22544928
PMCPMC3758685
OpenAlexW1927035308

What OpenQuestion holds

Textmetadata
LicenceTDM
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.