Evidence map›Paper›PMID 30088364›Full record

ReviewAllergy, asthma & immunology research2018

Autoimmune Responses in Severe Asthma.

Manali Mukherjee, Parameswaran Nair

Open access · bronzeAbstract readReview
In one paragraph

Review in Allergy, asthma & immunology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% 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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. Pooled it
  2. Autoallergy in chronic rhinosinusitis and its clinical relevance.The World Allergy Organization journal · 2026
    Article
  3. One size does not fit all: uncontrolled T2 inflammation on tezepelumab-a case series.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Bark Extracts ofPlants (Basel, Switzerland) · 2025
    Article
  8. Comorbidities in Canadian patients with hereditary angioedema: a quantitative survey study.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. IL-18 biology in severe asthma.Frontiers in medicine · 2024
    Review
  17. Article
  18. Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Manali MukherjeeDivision of Respirology, Department of Medicine, St. Joseph's Healthcare Hamilton, McMaster University, Hamilton, Canada.
Parameswaran NairDivision of Respirology, Department of Medicine, St. Joseph's Healthcare Hamilton, McMaster University, Hamilton, Canada. parames@mcmaster.ca.
St. Joseph’s Healthcare Hamilton · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Asthma and autoimmune diseases both result from a dysregulated immune system, and have been conventionally considered to have mutually exclusive pathogenesis. Autoimmunity is believed to be an exaggerated Th1 response, while asthma with a Th2 underpinning is congruent with the well-accepted Th1/Th2 paradigm. The hypothesis of autoimmune involvement in asthma has received much recent interest, particularly in the adult late-onset non-atopic patients (the "intrinsic asthma"). Over the past decades, circulating autoantibodies against diverse self-targets (beta-2-adrenergic receptors, epithelial antigens, nuclear antigens, etc.) have been reported and subsequently dismissed to be epiphenomena resulting from a chronic inflammatory condition, primarily due to lack of evidence of causality/pathomechanism. Recent evidence of 'granulomas' in the lung biopsies of severe asthmatics, detection of pathogenic sputum autoantibodies against autologous eosinophil proteins (e.g., eosinophil peroxidase) and inadequate response to monoclonal antibody therapies (e.g., subcutaneous mepolizumab) in patients with evidence of airway autoantibodies suggest that the role of autoimmune mechanisms be revisited. In this review, we have gathered available reports of autoimmune responses in the lungs, reviewed the evidence in the context of immunogenic tissue-response and danger-associated molecular patterns, and constructed the possibility of an autoimmune-associated pathomechanism that may contribute to the severity of asthma.

Indexed as

Autoantibodiesautoimmunitydanger associated molecular patternsdegranulationimmunoglobulin Gneutrophilssevere asthmasputumsputum eosinophils

Identifiers

PMID30088364
PMCPMC6082822
OpenAlexW2886563812

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.