ReviewGenes2017
The Genetic Architecture of Type 1 Diabetes.
Review in Genes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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.
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.
Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Maternal Autoimmune Disease and Childhood-Onset Type 1 Diabetes: A Nationwide Population-Based Nested Case-Control Study.Pediatric diabetes · 2026Article
- Stable heritability of type 1 diabetes in a Swedish Nationwide Cohort Study.Nature communications · 2025Article
- Implication of the HLA-DQA1, HLA-DQB1 and CTLA-4 alleles in the susceptibility to type 1 diabetes in Jordanian population.Molecular biology reports · 2025Article
- Disease-modifying pharmacological treatments of type 1 diabetes: Molecular mechanisms, target checkpoints, and possible combinatorial treatments.Pharmacological reviews · 2025Review
- Stem Cell Therapy for the Management of Type 1 Diabetes: Advances and Perspectives.Endocrine, metabolic & immune disorders drug targets · 2024Review
- Abatacept increases T cell exhaustion in early RA individuals who carry HLA risk alleles.Frontiers in immunology · 2024Article
- Longitudinal changes in DNA methylation during the onset of islet autoimmunity differentiate between reversion versus progression of islet autoimmunity.Frontiers in immunology · 2024Article
- Anti-Idiotypic mRNA Vaccine to Treat Autoimmune Disorders.Vaccines · 2023Review
- Methylation haplotypes of the insulin gene promoter in children and adolescents with type 1 diabetes: Can a dimensionality reduction approach predict the disease?Experimental and therapeutic medicine · 2023Article
- Important denominator between autoimmune comorbidities: a review of class II HLA, autoimmune disease, and the gut.Frontiers in immunology · 2023Review
- Setting the Stage for Insulin Granule Dysfunction during Type-1-Diabetes: Is ER Stress the Culprit?Biomedicines · 2022Review
- The missing heritability in type 1 diabetes.Diabetes, obesity & metabolism · 2022Review
- Association and Familial Coaggregation of Childhood-Onset Type 1 Diabetes With Depression, Anxiety, and Stress-Related Disorders: A Population-Based Cohort Study.Diabetes care · 2022Article
- Impact of land use and food environment on risk of type 2 diabetes: A national study of veterans, 2008-2018.Environmental research · 2022Article
- High-risk genotypes for type 1 diabetes are associated with the imbalance of gut microbiome and serum metabolites.Frontiers in immunology · 2022Article
- Sib-pair subgroup familial type 1 diabetes mellitus in children in the state of Qatar.PloS one · 2022Article
- Localization of enteroviral RNA within the pancreas in donors with T1D and T1D-associated autoantibodies.Cell reports. Medicine · 2021Article
- Insights fromMicroorganisms · 2021Article
- Epigenetic Changes Induced by Maternal Factors during Fetal Life: Implication for Type 1 Diabetes.Genes · 2021Review
- Haploinsufficiency of theJournal of medical genetics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is classically characterised by the clinical need for insulin, the presence of disease-associated serum autoantibodies, and an onset in childhood. The disease, as with other autoimmune diseases, is due to the interaction of genetic and non-genetic effects, which induce a destructive process damaging insulin-secreting cells. In this review, we focus on the nature of this interaction, and how our understanding of that gene-environment interaction has changed our understanding of the nature of the disease. We discuss the early onset of the disease, the development of distinct immunogenotypes, and the declining heritability with increasing age at diagnosis. Whilst Human Leukocyte Antigens (HLA) have a major role in causing T1D, we note that some of these HLA genes have a protective role, especially in children, whilst other non-HLA genes are also important. In adult-onset T1D, the disease is often not insulin-dependent at diagnosis, and has a dissimilar immunogenotype with reduced genetic predisposition. Finally, we discuss the putative nature of the non-genetic factors and how they might interact with genetic susceptibility, including preliminary studies of the epigenome associated with T1D.
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What OpenQuestion holds
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.