Evidence map›Paper›PMID 33101299›Full record

ReviewFrontiers in immunology2020

Insights Into Type I and III Interferons in Asthma and Exacerbations.

Helen E Rich, Danielle Antos, Natalie R Melton, John F Alcorn, Michelle L Manni

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 5% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. Article
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  12. Article
  13. Article
  14. The role of innate immune system in respiratory viral infection related asthma.Frontiers in cellular and infection microbiology · 2025
    Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. PANoptosis: Mechanism and Role in Pulmonary Diseases.International journal of molecular sciences · 2023
    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.

Helen E RichDepartment of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
Danielle AntosDepartment of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
Natalie R MeltonDepartment of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
John F AlcornDepartment of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
Michelle L ManniDepartment of Pediatrics, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, United States.
Children's Hospital of Pittsburgh · US

Funding

Immune Mediators of IL-22 Signaling Alter Allergic Airway DiseaseR01HL146445 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MANNI, MICHELLE LYNN · 2020 to 2024
$2.1M
NHLBI NIH HHS R01 HL146445
6 · The paper itself

Abstract

Asthma is a highly prevalent, chronic respiratory disease that impacts millions of people worldwide and causes thousands of deaths every year. Asthmatics display different phenotypes with distinct genetic components, environmental causes, and immunopathologic signatures, and are broadly characterized into type 2-high or type 2-low (non-type 2) endotypes by linking clinical characteristics, steroid responsiveness, and molecular pathways. Regardless of asthma severity and adequate disease management, patients may experience acute exacerbations of symptoms and a loss of disease control, often triggered by respiratory infections. The interferon (IFN) family represents a group of cytokines that play a central role in the protection against and exacerbation of various infections and pathologies, including asthma. Type I and III IFNs in particular play an indispensable role in the host immune system to fight off pathogens, which seems to be altered in both pediatric and adult asthmatics. Impaired IFN production leaves asthmatics susceptible to infection and with uncontrolled type 2 immunity, promotes airway hyperresponsiveness (AHR), and inflammation which can lead to asthma exacerbations. However, IFN deficiency is not observed in all asthmatics, and alterations in IFN expression may be independent of type 2 immunity. In this review, we discuss the link between type I and III IFNs and asthma both in general and in specific contexts, including during viral infection, co-infection, and bacterial/fungal infection. We also highlight several studies which examine the potential role for type I and III IFNs as asthma-related therapies.

Indexed as

AsthmaBacteriaFungiHumansImmunomodulationInterferonsLungRespiratory Tract InfectionsT-Lymphocytes, Helper-InducerVirusesInterferonsasthmaasthma therapeuticsinfectioninterferon-alphainterferon-betainterferon-lambdatype III interferontype I interferon

Identifiers

PMID33101299
PMCPMC7546400
OpenAlexW3087933914

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.