Evidence map›Paper›PMID 34364539›Full record

ReviewThe Journal of allergy and clinical immunology2021

Innate immune cell dysregulation drives inflammation and disease in aspirin-exacerbated respiratory disease.

Ryan Eid, Carol H Yan, Whitney Stevens, Taylor A Doherty, Larry Borish

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Aspirin-Derived Salicyl-CoA Drives Histone Lysine Salicylation Regulated by CBP and SIRT2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Review
  3. Group 2 innate lymphoid cells: Where are we 15 years out?The Journal of allergy and clinical immunology · 2026
    Review
  4. Dupilumab Dampens Mucosal Type 2 Response During Acetylsalicylic Acid Challenge in N-ERD Patients.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2026
    Article
  5. Article
  6. Article
  7. Immune endotyping and gene expression profile of patients with chronic rhinosinusitis with nasal polyps in the aspirin-exacerbated respiratory disease (AERD) and the non-AERD subgroups.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2024
    Article
  8. Progestogen Hypersensitivity.The journal of allergy and clinical immunology. In practice · 2023
    Article
  9. Article
  10. Aspirin-exacerbated respiratory disease: Updates in the era of biologics.Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology · 2023
    Review
  11. 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

5 authors at 3 institutions in 1 country.

Ryan EidDepartment of Medicine, University of Virginia Health System, Charlottesville, Va.
Carol H YanDepartment of Surgery, Division of Otolaryngology-Head and Neck Surgery, University of California, San Diego, San Diego, Calif.
Whitney StevensDepartment of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Ill; Department of Otolaryngology, Northwestern University Feinberg School of Medicine, Chicago, Ill.
Taylor A DohertyDepartment of Medicine, Division of Rheumatology, Allergy and Immunology, University of California, San Diego, Calif; Veterans Affairs San Diego Health Care System, La Jolla, Calif.
Larry BorishDepartment of Medicine, University of Virginia Health System, Charlottesville, Va; Department of Microbiology, University of Virginia Health System, Charlottesville, Va. Electronic address: lb4m@virginia.edu.
University of California, San Diego · USUniversity of Virginia Health System · USNorthwestern University · US

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
Clinical response to rhinovirus challenge in human asthmaticsU01AI123337 · NIAID · UNIVERSITY OF VIRGINIA · PI BORISH, LARRY C · 2016 to 2020
$3.6M
Clinical Centers for the NHLBI's Precision Interventions for Severe and/or Exacerbation Prone Asthma (PrecISE) Network (UG1)UG1HL139126 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI ERZURUM, SERPIL C., GASTON, BENJAMIN · 2017 to 2022
$2.4M
Mentoring patient-oriented researchers in inflammatory airway diseaseK24AI171795 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAYLOR A DOHERTY · 2022 to 2026
$968k
Cellular and Molecular Mechanisms of the Pathogenesis of Aspirin Exacerbated Respiratory DiseaseK23AI141694 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI STEVENS, WHITNEY W · 2019 to 2023
$948k
Lung rhinovirus (RV) infection identifies pre-school children with type 2 inflammation at risk for the development of asthmaR21AI151496 · NIAID · UNIVERSITY OF VIRGINIA · PI BORISH, LARRY C, TEAGUE, WILLIAM GERALD · 2020 to 2021
$444k
Targeting pathogenic innate lymphoid cells in airway diseaseI01BX005073 · VA · VA SAN DIEGO HEALTHCARE SYSTEM · PI TAYLOR A DOHERTY · 2021 to 2026
–
BLRD VA I01 BX005073NHLBI NIH HHS UG1 HL139126NIAID NIH HHS K23 AI141694NIAID NIH HHS K24 AI171795NIAID NIH HHS R21 AI151496NIAID NIH HHS U01 AI123337NIAID NIH HHS U19 AI070535
6 · The paper itself

Abstract

Aspirin-exacerbated respiratory disease (AERD) is a complex inflammatory disorder that is not generally viewed as a disease involving the adaptive immune system but instead one largely driven by the innate immune system. This article focuses on the cellular dysregulation involving 4 central cell types: eosinophils, basophils, mast cells, and innate lymphoid type 2 cells. AERD can be envisioned as involving a self-perpetuating vicious circle in which mediators produced by a differentiated activated epithelial layer, such as IL-25, IL-33, and thymic stromal lymphopoietin, engage and activate each of these innate immune cells. The activation of these innate immune cells with their production of additional cytokine/chemokine and lipid mediators leads to further recruitment and activation of these innate immune cells. More importantly, numerous mediators produced by these innate immune cells provoke the epithelium to induce further inflammation. This self-perpetuating cycle of inflammation partially explains both current interventions suggested to ameliorate AERD (eg, aspirin desensitization, leukotriene modifiers, anti-IL-5/IL-5 receptor, anti-IL-4 receptor, and anti-IgE) and invites exploration of novel targets as specific therapies for this condition (prostaglandin D

Indexed as

AnimalsAspirinAsthma, Aspirin-InducedCytokinesHumansImmunity, InnateInflammationLeukocytesAspirinCytokinesAspirin-exacerbated respiratory diseasebasophilseosinophilsIgEinnate lymphoid cellsmast cellstype 2 inflammation

Identifiers

PMID34364539
PMCPMC8363117
OpenAlexW3187748752

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.