Evidence map›Paper›PMID 27913952›Full record

ReviewInflammation2017

Association of interleukin-18 and asthma.

Ming-Hui Xu, Feng-Lai Yuan, Shu-Jing Wang, Hui-Ying Xu, Cheng-Wan Li, Xiao Tong

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation, 2017. 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
–field-weighted citation impact
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.

  1. Interleukin-18 armours antitumour immune effectors.Nature reviews. Immunology · 2026
    Review
  2. Article
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  7. Review
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  14. A comprehensive pathway map of IL-18-mediated signalling.Journal of cell communication and signaling · 2020
    Article
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  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

6 authors.

Ming-Hui XuDepartment of Pediatrics, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu, 214041, China.
Feng-Lai YuanDepartment of Pediatrics, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu, 214041, China.
Shu-Jing WangDepartment of Pediatrics, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu, 214041, China.
Hui-Ying XuDepartment of Pediatrics, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu, 214041, China.
Cheng-Wan LiDepartment of Pediatrics, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu, 214041, China. lichengwan1965@163.com.
Xiao TongDepartment of Pediatrics, The Third Hospital Affiliated to Nantong University, Wuxi, Jiangsu, 214041, China. drtong@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytokine-mediated immunity plays a dominant role in the pathogenesis of various immune diseases, including asthma. The recent identification of the family interleukin (IL)-1-related cytokine IL-18 now contributes to our understanding of the fine-tuning of cellular immunity. IL-18 can act as a cofactor for Th2 cell development and IgE production and also plays an important role in the differentiation of Th1 cells. Recent work identified an IL-18 association with the pathogenesis of asthma, wherein increased IL-18 expression was found in the serum of patients. Furthermore, IL-18 polymorphisms with susceptibility to asthma were reported, suggesting that IL-18 may be therapeutically relevant to asthma. In this review, we discuss the role of IL-18 in the pathogenesis of asthma and its therapeutic potential based on current research.

Indexed as

AsthmaCytokinesHumansInterleukin-18T-Lymphocytes, Helper-InducerCytokinesInterleukin-18AsthmaIL-18Th1 cellTh2 cell

Identifiers

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.