Evidence map›Paper›PMID 22069270›Full record

ArticleDiabetes/metabolism research and reviews2011

Genetic association analyses of atopic illness and proinflammatory cytokine genes with type 1 diabetes.

Nada M Saleh, Srilakshmi M Raj, Deborah J Smyth, Chris Wallace, Joanna M M Howson, Louise Bell, Neil M Walker, Helen E Stevens, John A Todd

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes/metabolism research and reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 52 citations in OpenAlex.

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  11. Pyroptosis, metabolism, and tumor immune microenvironment.Clinical and translational medicine · 2021
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  14. Genetic Regulation of Immunoglobulin G Glycosylation.Experientia supplementum (2012) · 2021
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  19. A decade of research on the 17q12-21 asthma locus: Piecing together the puzzle.The Journal of allergy and clinical immunology · 2018
    Review
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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

9 authors at 1 institution in 1 country.

Nada M SalehJuvenile Diabetes Research Foundation/Wellcome Trust Diabetes and Inflammation Laboratory, Department of Medical Genetics, Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 0XY, UK.
Srilakshmi M Raj
Deborah J Smyth
Chris Wallace
Joanna M M Howson
Louise Bell
Neil M Walker
Helen E Stevens
John A Todd
University of Cambridge · GB

Funding

British Heart Foundation RG/08/014/24067Medical Research Council G0000934Wellcome Trust 068545/Z/02Wellcome Trust 076113/C/04/ZWellcome Trust 079895Wellcome Trust 089989Wellcome Trust 091157Wellcome Trust WT061858
6 · The paper itself

Abstract

backgroundThe genetic basis of the autoimmune disease type 1 diabetes (T1D) has now been largely determined, so now we can compare these findings with emerging genetic knowledge of disorders and phenotypes that have been negatively or positively associated with T1D historically. Here, we assessed the role in T1D of variants previously reported to be associated with atopic diseases and epithelial barrier function, profilaggrin (FLG), and those that affect the expression levels of the proinflammatory cytokines tumour necrosis factor (TNF)-α, interleukin (IL)-1β, interferon (IFN)γ and IL-18.

methodsWe genotyped single nucleotide polymorphisms (SNPs): -105/rs28665122 in SELS or SEPS1 (selenoprotein), three single nucleotide polymorphisms in IL18 (-105/rs360717, +183/rs5744292 and +1467/rs574456) and R501X/rs61816761 in FLG, the major locus associated with atopic dermatitis and predisposing to asthma, in a minimum of 6743 T1D cases and 7864 controls.

resultsNo evidence of T1D association was found for any of the SNPs we genotyped at FLG, SELS or IL18 (p≥0.03), nor with haplotypes of IL18 (p=0.82). Review of previous T1D genome-wide association results revealed that four (human leucocyte antigen (HLA), gasdermin B/ORM1 (Saccharomyces cerevisiae)-like/gasdermin B/, GSDMB/ORMDL3/GSDMA and IL2RB) of ten loci recently reported to be associated with asthma were associated with T1D (p≤0.005).

conclusionsThese results show that there are shared genetic associations for atopy-related traits and T1D, and this might help in the future to understand the mechanisms, pathways and environmental factors that underpin the rapid rise in incidence of both disorders in children.

Indexed as

AsthmaChildDiabetes Mellitus, Type 1Filaggrin ProteinsGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansHypersensitivity, ImmediateInterferon-gammaInterleukin-18Intermediate Filament ProteinsMembrane ProteinsPolymorphism, Single NucleotideSelenoproteinsTumor Necrosis Factor-alphaFilaggrin ProteinsFLG protein, humanInterferon-gammaInterleukin-18Intermediate Filament ProteinsMembrane ProteinsSelenoproteinsSELENOS protein, humanTumor Necrosis Factor-alpha

Identifiers

PMID22069270
PMCPMC3816329
OpenAlexW2127227773

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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.