Evidence map›Paper›PMID 31057533›Full record

ReviewFrontiers in immunology2019

IL-33 Mediated Inflammation in Chronic Respiratory Diseases-Understanding the Role of the Member of IL-1 Superfamily.

Agata Gabryelska, Piotr Kuna, Adam Antczak, Piotr Białasiewicz, Michał Panek

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
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  5. Air pollution-induced airway epithelial barrier dysfunction in COPD: a narrative review of mechanisms and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Targeting alarmins in asthma: From bench to clinic.The Journal of allergy and clinical immunology · 2025
    Review
  14. Article
  15. Review
  16. Review
  17. Epithelial Interleukin-1 Receptor-Like-1 Activation Is Contingent on Interleukin-33 Isoforms and Asthma-Related Receptor Variation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2024
    Article
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  20. Article

9 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

5 authors at 1 institution in 1 country.

Agata GabryelskaDepartment of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Łódz, Poland.
Piotr KunaDepartment of Internal Medicine, Asthma and Allergy, Medical University of Lodz, Łódz, Poland.
Adam AntczakDepartment of General and Oncological Pulmonology, Medical University of Lodz, Łódz, Poland.
Piotr BiałasiewiczDepartment of Sleep Medicine and Metabolic Disorders, Medical University of Lodz, Łódz, Poland.
Michał PanekDepartment of Internal Medicine, Asthma and Allergy, Medical University of Lodz, Łódz, Poland.
Medical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin 33 (IL-33) is an alarmin cytokine from the IL-1 family. IL-33 is localized in the nucleus and acts there as a gene regulator. Following injury, stress or cell death, it is released from the nucleus, and exerts its pro-inflammatory biological functions via the transmembrane form of the ST2 receptor, which is present mainly as attached to immune cells. In recent years, IL-33 became a focus of many studies due to its possible role in inflammatory disorders. Among respiratory disorders, the contribution of IL-33 to the development of asthma, in particular, has been most identified. Increased level of IL-33 in lung epithelial cells and blood serum has been observed in asthma patients. The IL-33/ST2 interaction activated the Th2 mediated immune response and further production of many pro-inflammatory cytokines. Single nucleotide polymorphisms in the IL-33 gene cause a predisposition to the development of asthma. Similarly, in chronic pulmonary obstructive disease (COPD), both increased expression of IL-33 and the ST2 receptor has been observed. Interestingly, cigarette smoke, a key inducer of COPD, not only activates IL-33 production by epithelial and endothelial cells, but also induces the expression of IL-33 in peripheral blood mononuclear cells. Knowledge regarding its contribution in other respiratory disorders, such as obstructive sleep apnea, remains greatly limited. Recently it was shown that IL-33 is one of the inflammatory mediators by which levels in blood serum are increased in OSA patients, compared to healthy control patients. This mini review summarizes current knowledge on IL-33 involvement in chosen chronic respiratory disorders and proposes this interleukin as a possible link in the pathogenesis of these diseases.

Indexed as

AnimalsAsthmaHumansInflammation MediatorsInterleukin-33Pulmonary Disease, Chronic ObstructiveSleep Apnea, ObstructiveIL33 protein, humanInflammation MediatorsInterleukin-33asthmaCOPD—Chronic obstructive pulmonary diseaseIL-33inflammationOSA (Obstructive sleep apnea)

Identifiers

PMID31057533
PMCPMC6477074
OpenAlexW2935954941

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.