Evidence map›Paper›PMID 29676014›Full record

ReviewImmunology2018

Autoinflammatory disease in the lung.

Thomas Scambler, Jonathan Holbrook, Sinisa Savic, Michael F McDermott, Daniel Peckham

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 36 citations in OpenAlex.

  1. Trial
  2. Review
  3. A translational view of airway epithelial dysfunction in COPD.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
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  10. Article
  11. Review
  12. Review
  13. Review
  14. EMC. Pediatria · 2020
    Review
  15. Review
  16. Review
  17. Article
  18. 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 2 institutions in 1 country.

Thomas ScamblerLeeds Institute of Rheumatic and Musculoskeletal Medicine, St James's University Hospital, Leeds, UK.
Jonathan HolbrookLeeds Institute of Rheumatic and Musculoskeletal Medicine, St James's University Hospital, Leeds, UK.
Sinisa SavicLeeds Institute of Rheumatic and Musculoskeletal Medicine, St James's University Hospital, Leeds, UK.
Michael F McDermottLeeds Institute of Rheumatic and Musculoskeletal Medicine, St James's University Hospital, Leeds, UK.
Daniel PeckhamCystic Fibrosis Trust Strategic Research Centre, St James's University Hospital, Leeds, UK.
St James's University Hospital · GBCystic Fibrosis Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ascertaining the dominant cell type driving an immunological disease is essential to understanding the causal pathology and, therefore, selecting or developing an effective treatment. Classifying immunological diseases in this way has led to successful treatment regimens for many monogenic diseases; however, when the dominant cell type is unclear and there is no obvious causal genetic mutation, then identifying the correct disease classification and appropriate therapy can be challenging. In this review we focus on pulmonary immunological diseases where an innate immune signature has been identified as a predominant aspect of the immunopathology. We describe the molecular pathology of 'autoinflammatory diseases of the lung' and propose that small molecule and biological therapies, including recombinant interleukin-1 receptor antagonist, that target key innate immune pathways, are likely be beneficial in the control of pulmonary and systemic inflammation in these conditions. In addition, the successful use of macrolide antibiotics to treat lung infections in these conditions further confirms that the innate immune system is the key conductor of inflammation in these pulmonary diseases, as there is a strong body of evidence that macrolides are able to modulate the NLRP3 inflammasome and interleukin-1β and interleukin-18 secretion, both of which are central players in the innate immune response. Throughout this review we highlight the published evidence of autoinflammatory disease in chronic obstructive pulmonary disease, bronchiectasis, cystic fibrosis and rheumatoid lung disease and suggest that the fundamental pathology of these diseases places them towards the autoinflammatory pole of the immunological disease continuum.

Indexed as

autoimmunitybronchiectasisCOPDcystic fibrosisinflammationpanbronchiolitis

Identifiers

PMID29676014
PMCPMC6050210
OpenAlexW2801684403

What OpenQuestion holds

Textmetadata
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.