Evidence map›Paper›PMID 17067313›Full record

ArticleImmunology2006

A dominant role for chemoattractant receptor-homologous molecule expressed on T helper type 2 (Th2) cells (CRTH2) in mediating chemotaxis of CRTH2+ CD4+ Th2 lymphocytes in response to mast cell supernatants.

Shân L Gyles, Luzheng Xue, Elizabeth R Townsend, Frank Wettey, Roy Pettipher

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
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  5. Article
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  7. The prostaglandin DRespiratory research · 2018
    Review
  8. Review
  9. Review
  10. Targeting the PGDDrugs · 2017
    Review
  11. Efficacy and safety of setipiprant in seasonal allergic rhinitis: results from Phase 2 and Phase 3 randomized, double-blind, placebo- and active-referenced studies.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2017
    Article
  12. Usefulness of targeting lymphocyte Kv1.3-channels in the treatment of respiratory diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015
    Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. CRTH2 expression on T cells in asthma.Clinical and experimental immunology · 2010
    Article
  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

5 authors at 1 institution in 1 country.

Shân L GylesDepartment of Drug Discovery, Oxagen Ltd, Abingdon, Oxon, United Kingdom.
Luzheng Xue
Elizabeth R Townsend
Frank Wettey
Roy Pettipher
Oxagen (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human cultured mast cells, immunologically activated with immunoglobuin E (IgE)/anti-IgE, released a factor(s) that promoted chemotaxis of human CRTH2+ CD4+ T helper type 2 (Th2) lymphocytes. Mast cell supernatants collected at 20 min, 1 hr, 2 hr and 4 hr after activation caused a concentration-dependent increase in the migration of Th2 cells. The effect of submaximal dilutions of mast-cell-conditioned media was inhibited in a dose-dependent manner by ramatroban (IC50 = 96 nm), a dual antagonist of both the thromboxane-like prostanoid (TP) receptor and the chemoattractant receptor-homologous molecule expressed on Th2 cells (CRTH2), but not by the selective TP antagonist SQ29548, implicating CRTH2 in mediating the chemotactic response of these Th2 cells. The effect of mast-cell-conditioned media was mimicked by prostaglandin D2 (PGD2) and this eicosanoid was detected in the conditioned media from activated mast cells in concentrations sufficient to account for the activity of the mast cell supernatants. Treatment of the mast cells with the cyclo-oxygenase inhibitor diclofenac (10 microm) inhibited both the production of PGD2 and the CRTH2+ CD4+ Th2-stimulatory activity, while addition of exogenous PGD2 to conditioned media from diclofenac-treated mast cells restored the ability of the supernatants to promote chemotaxis of these Th2 cells. The degree of inhibition caused by diclofenac treatment of the mast cells was concordant with the degree of inhibition of chemotactic responses afforded by CRTH2 blockade. These data suggest that PGD2, or closely related metabolites of arachidonic acid, produced from mast cells may play a central role in the activation of CRTH2+ CD4+ Th2 lymphocytes through a CRTH2-dependent mechanism.

Indexed as

CarbazolesCells, CulturedChemotaxis, LeukocyteCulture Media, ConditionedCyclooxygenase InhibitorsDiclofenacDose-Response Relationship, ImmunologicHumansImmunoglobulin ELymphocyte ActivationMast CellsProstaglandin D2Receptors, ImmunologicReceptors, ProstaglandinReceptors, ThromboxaneSulfonamidesCarbazolesCulture Media, ConditionedCyclooxygenase InhibitorsDiclofenacImmunoglobulin EProstaglandin D2prostaglandin D2 receptorramatrobanReceptors, ImmunologicReceptors, ProstaglandinReceptors, ThromboxaneSulfonamides

Identifiers

PMID17067313
PMCPMC1819579
OpenAlexW2006698613

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.