Evidence map›Paper›PMID 17919738›Full record

ReviewImmunology letters2007

G protein-coupled receptors and the modification of FcepsilonRI-mediated mast cell activation.

Hye Sun Kuehn, Alasdair M Gilfillan

Open access · greenAbstract readReview
In one paragraph

Review in Immunology letters, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

61 citing papers in PubMed, 116 citations in OpenAlex.

  1. Stromal Cell-Mast Cell Communication Orchestrates Anti-Viral Immunity in the Meninges.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. Impact of TNF and IL-33 Cytokines on Mast Cells in Neuroinflammation.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Catechin synergistically potentiates mast cell-stabilizing property of caffeine.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2021
    Article
  9. Article
  10. Article
  11. Environmental and Endogenous Acids Can Trigger Allergic-Type Airway Reactions.International journal of environmental research and public health · 2020
    Review
  12. Article
  13. PI3KFrontiers in immunology · 2020
    Article
  14. BioMed research international · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

1 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

2 authors at 2 institutions in 1 country.

Hye Sun KuehnLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892-1881, USA.
Alasdair M Gilfillan
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Integrated Signaling Pathways for the Enhancement of Mast Cell ActivationZ01AI000965 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI METCALFE, DEAN D · 2006 to 2008
$772k
Intramural NIH HHS Z01 AI000965
6 · The paper itself

Abstract

By releasing multiple pro-inflammatory mediators upon activation, mast cells are critical effector cells in the pathogenesis of allergic inflammation. The traditional viewpoint of antigen-dependent mast cell activation is that of a Th(2)-driven process whereby antigen-specific IgE molecules are produced by B cells followed by binding of the IgE to high affinity IgE receptors (FcepsilonRI) expressed on mast cells. Subsequent antigen-dependent aggregation of the FcepsilonRI initiates an intracellular signalling cascade that culminates in mediator release. Mast cell responses, including cell growth, survival, chemotaxis, and cell adhesion, however, can also be regulated by other receptors expressed on mast cells. Furthermore, FcepsilonRI-mediated mast cell mediator release can be significantly modified by ligation of specific classes of these receptors. One such class of receptors is the G protein-coupled receptors (GPCR). In this review, we describe how sub-populations of GPCRs can either enhance or inhibit FcepsilonRI-mediated mast cell activation depending on the particular G protein utilized for relaying signalling. Furthermore, we discuss the potential mechanisms whereby the signalling responses utilized by the FcepsilonRI for mast cell activation are influenced by those initiated by GPCRs to produce these diverse responses.

Indexed as

AnimalsCell DegranulationChemokinesHumansImmunoglobulin ELigandsMast CellsReceptor AggregationReceptors, G-Protein-CoupledReceptors, IgESignal TransductionChemokinesImmunoglobulin ELigandsReceptors, G-Protein-CoupledReceptors, IgE

Identifiers

PMID17919738
PMCPMC2094129
OpenAlexW2022660538

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.