Evidence map›Paper›PMID 17215860›Full record

ReviewGenes and immunity2007

Interleukin-18 genetics and inflammatory disease susceptibility.

S R Thompson, S E Humphries

Abstract readReview
PubMed Publisher
In one paragraph

Review in Genes and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
2.8field-weighted citation impact, top 9% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 91 citations in OpenAlex.

  1. Associations between interleukin 18 gene polymorphisms and susceptibility to vasculitis: A meta-analysis.Sarcoidosis, vasculitis, and diffuse lung diseases : official journal of WASOG · 2020
    Pooled it
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  9. The risk of atopic dermatitis may be affected byPostepy dermatologii i alergologii · 2021
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  16. Molecular and clinical oncology · 2017
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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.

S R ThompsonThe Department of Cardiovascular Genetics, The Rayne Institute, London, UK.
S E Humphries

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL18 was mapped to 11q22.2-22.3 in 1998. Owing to interleukin (IL)-18's important and novel role in immunomodulation, the gene itself has been subject to scrutiny, with the aim of discovering variants that may impact on disease susceptibility and/or progression. Despite being sequenced numerous times in different populations, no non-synonymous variants have been found. However, a number of polymorphisms within the proximal promoter have been verified that may interfere with transcription-factor-binding sites. Much of the subsequent association analyses have centred on these variants, but have yielded no consistent results, despite numerous different study populations being genotyped. IL18 has recently been resequenced in its entirety, enabling the tagging-single-nucleotide polymorphism (tSNP) methodology to be adopted. This approach has yielded interesting results, with genetic variation being shown to affect protein levels, and risk. This review aims to compile and reflect on the association data of interest published to date, with a focus on the diseases related to aberrant inflammatory control.

Indexed as

Genetic VariationArthritisAsthmaAtherosclerosisDiabetes Mellitus, Type 1Gene Expression RegulationGenetic Predisposition to DiseaseGraft vs Host DiseaseHumansInflammationInflammatory Bowel DiseasesInterleukin-18Multiple SclerosisPolymorphism, Single NucleotideSignal TransductionInterleukin-18

Identifiers

PMID17215860
OpenAlexW1981116369

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.