Evidence map›Paper›PMID 39462122›Full record

ArticleScientific reports2024

Risk of celiac disease autoimmunity is modified by interactions between CD247 and environmental exposures.

Anna Eurén, Kristian Lynch, Katri Lindfors, Hemang Parikh, Sibylle Koletzko, Edwin Liu, Beena Akolkar, William Hagopian, Jeffrey Krischer, Marian Rewers and 5 more

Registry-linked trialAbstract readMulticenter Study
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT00279318 (Consortium for Identification of Environmental Triggers of Type 1 Diabetes), which is not on this map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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.

NCT00279318 completednot on this map

Consortium for Identification of Environmental Triggers of Type 1 Diabetes

TypeobservationalSponsorNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Ran2004 to 2025Enrolled8,667ConditionsType 1 Diabetes Mellitus
3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. 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

15 authors.

Anna EurénCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Kristian LynchHealth Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Katri LindforsCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland.
Hemang ParikhHealth Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Sibylle KoletzkoDr. von Hauner Children's Hospital, Department of Pediatrics, University Hospital, LMU Munich, Munich, Germany.
Edwin LiuDigestive Health Institute, Children's Hospital, Anschutz Medical Campus, University of Colorado, Denver, CO, USA.
Beena AkolkarNational Institute of Diabetes & Digestive & Kidney Diseases, Bethesda, MD, USA.
William HagopianDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
Jeffrey KrischerHealth Informatics Institute, Morsani College of Medicine, University of South Florida, Tampa, FL, USA.
Marian RewersBarbara Davis Center for Childhood Diabetes, University of Colorado, Denver, CO, USA.
Jorma ToppariInstitute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, and Centre for Population Health Research, University of Turku, Turku, Finland.
Anette ZieglerInstitute of Diabetes Research, Helmholtz Zentrum München, Munich, Germany.
Daniel AgardhLund University, Lund, Sweden.
Kalle KurppaCeliac Disease Research Center, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland. kalle.kurppa@tuni.fi.ORCID http://orcid.org/0000-0003-4757-2164
TEDDY Study Group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Season of birth, viral infections, HLA haplogenotypes and non-HLA variants are implicated in the development of celiac disease and celiac disease autoimmunity, suggesting a combined role of genes and environmental exposures. The aim of the study was to further decipher the biological pathways conveying the season of birth effect in celiac disease autoimmunity to gain novel insights into the early pathogenesis of celiac disease. Interactions between season of birth, genetics, and early-life environmental factors on the risk of celiac autoimmunity were investigated in the multicenter TEDDY birth cohort study. Altogether 6523 genetically predisposed children were enrolled to long-term follow-up with prospective sampling and data collection at six research centers in the USA, Germany, Sweden and Finland. Celiac disease autoimmunity was defined as positive tissue transglutaminase antibodies in two consecutive serum samples. There was a significant season of birth effect on the risk of celiac autoimmunity. The effect was dependent on polymorphisms in CD247 gene encoding for CD3ζ chain of TCR-CD3 complex. In particular, children with major alleles for SNP rs864537A > G, in CD247 (AA genotype) had an excess risk of celiac autoimmunity when born March-August as compared to other months. The interaction of CD247 with season of birth on autoimmunity risk was accompanied by interactions with febrile infections between the ages of 3-6 months. Considering the important role of TCR-CD3 complex in the adaptive immune response and our findings here, CD247 variants and their possible effect of subgroups in autoimmunity development could be of interest in the design of future gene-environment studies of celiac disease. ClinicalTrials.gov Identifier: NCT00279318.

Indexed as

AutoimmunityCeliac DiseaseEnvironmental ExposureGenetic Predisposition to DiseasePolymorphism, Single NucleotideSeasonsBirth CohortCD3 ComplexChildChild, PreschoolFemaleGene-Environment InteractionHumansInfantMaleProspective StudiesCD3 ComplexProtein Glutamine gamma Glutamyltransferase 2

Identifiers

PMID39462122
PMCPMC11567144

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Registered trials

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.