Evidence map›Paper›PMID 31587797›Full record

ReviewThe Journal of allergy and clinical immunology2019

Aspirin sensitivity: Lessons in the regulation (and dysregulation) of mast cell function.

Joshua A Boyce

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Mast Cells in Aspirin-Exacerbated Respiratory Disease.Current allergy and asthma reports · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Biomarkers for predicting response to aspirin therapy in aspirin-exacerbated respiratory disease.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
    Article
  10. Review
  11. Does IgE Have a Role in Aspirin-exacerbated Respiratory Disease?American journal of respiratory and critical care medicine · 2020
    Article
  12. Review
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

1 author at 1 institution in 1 country.

Joshua A BoyceDivision of Allergy and Clinical Immunology, Brigham and Women's Hospital, Boston, Mass. Electronic address: jboyce@rics.bwh.harvard.edu.
Brigham and Women's Hospital · US

Funding

Therapeutic Control of Aspirin-Exacerbated Respiratory DiseaseU19AI095219 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Joshua A Boyce · 2011 to 2026
$29.1M
Role of PGE2 in Human Mast Cell BiologyP01HL036110 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LAM, BING K · 1985 to 2009
$20.1M
Regulation of Pulmonary Prostaglandins by Leukotriene E4R01AI078908 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2009 to 2025
$8.8M
Eicosanoid Networks in Aspirin HypersensitivityR01AI136041 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Joshua A Boyce · 2018 to 2026
$5.4M
CysLT and P2Y Receptors in Lung InflammationR37AI052353 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2013 to 2022
$5.2M
CystLT and P2Y Receptors and Lung InflammationR01AI052353 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BOYCE, JOSHUA A · 2002 to 2012
$4.2M
Optimizing EP receptor subtype targeting for asthma therapyR01HL136209 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI BIRRELL, MARK A, BOYCE, JOSHUA A · 2017 to 2020
$2.2M
NHLBI NIH HHS P01 HL036110NHLBI NIH HHS R01 HL136209NIAID NIH HHS R01 AI052353NIAID NIH HHS R01 AI078908NIAID NIH HHS R01 AI136041NIAID NIH HHS R37 AI052353NIAID NIH HHS U19 AI095219
6 · The paper itself

Abstract

The idiosyncratic activation of mast cells (MCs) in response to administration of nonselective COX inhibitors is a cardinal feature of aspirin-exacerbated respiratory disease (AERD). Older studies using MC-stabilizing drugs support a critical role for MCs and their products in driving the severe eosinophilic inflammation and respiratory dysfunction that is typical of AERD. Because patients with AERD react to all nonselective COX inhibitors regardless of their chemical structure, the mechanism of MC activation is not caused by classical, antigen-induced cross-linking of IgE receptors. Recent studies in both human subjects and animal models have revealed a complex and multifactorial process culminating in dysregulation of MC function and an aberrant dependency on COX-1-derived prostaglandin E

Indexed as

AnimalsAsthma, Aspirin-InducedHumansMast CellsAspirinasthmaleukotrienesmast cellsprostaglandins

Identifiers

PMID31587797
PMCPMC7735393
OpenAlexW2977448480

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.