Evidence map›Paper›PMID 26405070›Full record

ArticleDiabetes care2015

Contrasting the Genetic Background of Type 1 Diabetes and Celiac Disease Autoimmunity.

Javier Gutierrez-Achury, Jihane Romanos, Sjoerd F Bakker, Vinod Kumar, Esther C de Haas, Gosia Trynka, Isis Ricaño-Ponce, Andrea Steck, Type 1 Diabetes Genetics Consortium, Wei-Min Chen and 8 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Diabetes care, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
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

26 citing papers in PubMed, 50 citations in OpenAlex.

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  15. Celiac Disease: Against the Grain in Gastroenterology.Journal of the Canadian Association of Gastroenterology · 2019
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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

18 authors at 5 institutions in 2 countries.

Javier Gutierrez-AchuryDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Jihane RomanosDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Sjoerd F BakkerDepartment of Gastroenterology and Hepatology, VU University Medical Centre, Amsterdam, the Netherlands.
Vinod KumarDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Esther C de HaasDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Gosia TrynkaDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Isis Ricaño-PonceDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands.
Andrea SteckBarbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO.
Type 1 Diabetes Genetics Consortium
Wei-Min ChenCenter for Public Health Genomics and Department of Public Health Sciences, School of Medicine, University of Virginia, Charlottesville, VA.
Suna Onengut-GumuscuCenter for Public Health Genomics and Department of Public Health Sciences, School of Medicine, University of Virginia, Charlottesville, VA.
Suat SimsekDepartment of Internal Medicine, Medical Center Alkmaar, Alkmaar, the Netherlands.
Diabeter
Marian RewersBarbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO.
Chris J MulderDepartment of Gastroenterology and Hepatology, VU University Medical Centre, Amsterdam, the Netherlands.
Ed LiuBarbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, CO.
Stephen S RichCenter for Public Health Genomics and Department of Public Health Sciences, School of Medicine, University of Virginia, Charlottesville, VA.
Cisca WijmengaDepartment of Genetics, University Medical Centre Groningen, University of Groningen, Groningen, the Netherlands c.wijmenga@umcg.nl.
University Medical Center Groningen · NLAmsterdam UMC Location Vrije Universiteit Amsterdam · NLUniversity of Virginia · USUniversity of Colorado Denver · USMedisch Centrum Alkmaar · NL

Funding

Type 1 Diabetes Genetics ConsortiumU01DK062418 · NIDDK · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICH, STEPHEN S. · 2002 to 2007
$59.8M
GENETIC AND ENVIRONMENTAL CAUSES OF CELIAC DISEASER01DK050979 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI REWERS, MARIAN J · 1995 to 2014
$4.0M
Characterizing the genetic architecture of childhood onset celiac disease using nR21DK084568 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LIU, EDWIN · 2009 to 2010
$766k
NIDDK NIH HHS 5R1-DK-084568-02NIDDK NIH HHS R01 DK050979NIDDK NIH HHS R21 DK084568NIDDK NIH HHS U01 DK062418Wellcome Trust
6 · The paper itself

Abstract

Type 1 diabetes (T1D) and celiac disease (CeD) cluster in families and can occur in the same individual. Genetic loci have been associated with susceptibility to both diseases. Our aim was to explore the genetic differences between individuals developing both these diseases (double autoimmunity) versus those with only one. We hypothesized that double autoimmunity individuals carry more of the genetic risk markers that are shared between the two diseases independently. SNPs were genotyped in loci associated with T1D (n=42) and CeD (n=28) in 543 subjects who developed double autoimmunity, 2,472 subjects with T1D only, and 2,223 CeD-only subjects. For identification of loci that were specifically associated with individuals developing double autoimmunity, two association analyses were conducted: double autoimmunity versus T1D and double autoimmunity versus CeD. HLA risk haplotypes were compared between the two groups. The CTLA4 and IL2RA loci were more strongly associated with double autoimmunity than with either T1D or CeD alone. HLA analyses indicated that the T1D high-risk genotype, DQ2.5/DQ8, provided the highest risk for developing double autoimmunity (odds ratio 5.22, P=2.25×10(-29)). We identified a strong HLA risk genotype (DQ2.5/DQ8) predisposing to double autoimmunity, suggesting a dominant role for HLA. Non-HLA loci, CTLA4 and IL2RA, may also confer risk to double autoimmunity. Thus, CeD patients who carry the DQ2.5/DQ8 genotype may benefit from periodic screening of autoantibodies related to T1D.

Indexed as

AutoimmunityCase-Control StudiesCeliac DiseaseCTLA-4 AntigenDiabetes Mellitus, Type 1FemaleGene FrequencyGenetic Association StudiesGenetic BackgroundGenetic LociGenetic Predisposition to DiseaseHaplotypesHLA AntigensHumansInterleukin-2 Receptor alpha SubunitLinkage DisequilibriumCTLA-4 AntigenCTLA4 protein, humanHLA AntigensIL2RA protein, humanInterleukin-2 Receptor alpha Subunit

Identifiers

PMID26405070
PMCPMC4582914
OpenAlexW2194453954

What OpenQuestion holds

Textmetadata
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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.