ReviewClinical chemistry2011
Genetics of type 1 diabetes.
Review in Clinical chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 5 of them syntheses that pooled 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.
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
150 citing papers in PubMed, 5 syntheses or guidelines pooled it, 310 citations in OpenAlex.
- Combined diabetic ketoacidosis and hyperosmolar hyperglycemic state in type 1 diabetes mellitus induced by immune checkpoint inhibitors: Underrecognized and underreported emergency in ICIs-DM.Frontiers in endocrinology · 2022Pooled it
- Double or hybrid diabetes: A systematic review on disease prevalence, characteristics and risk factors.Nutrition & diabetes · 2019Pooled it
- Immune checkpoint inhibitors and type 1 diabetes mellitus: a case report and systematic review.European journal of endocrinology · 2019Pooled it
- A systematic literature review on the European, African and Amerindian genetic ancestry components on Brazilian health outcomes.Scientific reports · 2019Pooled it
- Pooled it
- Plasma GAD65, a Marker for Early β-Cell Loss After Intraportal Islet Cell Transplantation in Diabetic Patients.The Journal of clinical endocrinology and metabolism · 2015Trial
- Euglycemic Diabetic Ketoacidosis Mimicking an Acute Asthma Exacerbation in a Young Adult With New-Onset Diabetes: A Case Report.Clinical case reports · 2026Article
- Gut microbiome maturation in early childhood interacts with host genetics to predict type 1 diabetes risk.Nature metabolism · 2026Article
- The Impact of Maternal Obesity and Diabetes on the Development of Congenital Heart Defects (CHDs) in Offspring: A Narrative Review.Metabolites · 2026Review
- Review
- Can we cure autoimmunity?Current opinion in immunology · 2026Review
- An Unprecedented Triad: Simultaneous Acute Pancreatitis, Axonal Polyneuropathy, and Type 1 Diabetes Mellitus in a Catastrophic Juvenile Lupus Flare.Clinical case reports · 2026Article
- ASTWAS: modeling alternative polyadenylation and SNP effects in kernel-driven TWAS reveal novel genetic associations for complex traits.Briefings in bioinformatics · 2026Article
- 14. Children and Adolescents: Standards of Care in Diabetes-2026.Diabetes care · 2026Review
- Article
- Pancreatic β-cell FFA2 deficiency suppresses multiple low dose streptozotocin induced diabetes in male mice.Communications biology · 2025Article
- Multiple low dose streptozotocin-induced diabetes as a model for studying autoimmune diabetes in humans.Animal models and experimental medicine · 2025Review
- A microRNA-based dynamic risk score for type 1 diabetes.Nature medicine · 2025Article
- Capturing dynamic rather than static risk for improved monitoring of type 1 diabetes progression.Nature medicine · 2025Article
- Utility of type 1 diabetes genetic risk score in a non-European population: insights from an Iranian cohort.Diabetology & metabolic syndrome · 2025Article
90 more citing papers are in PubMed but not listed here.
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
Abstract
backgroundType 1 diabetes, a multifactorial disease with a strong genetic component, is caused by the autoimmune destruction of pancreatic β cells. The major susceptibility locus maps to the HLA class II genes at 6p21, although more than 40 non-HLA susceptibility gene markers have been confirmed. CONTENT: Although HLA class II alleles account for up to 30%-50% of genetic type 1 diabetes risk, multiple non-MHC loci contribute to disease risk with smaller effects. These include the insulin, PTPN22, CTLA4, IL2RA, IFIH1, and other recently discovered loci. Genomewide association studies performed with high-density single-nucleotide-polymorphism genotyping platforms have provided evidence for a number of novel loci, although fine mapping and characterization of these new regions remain to be performed. Children born with the high-risk genotype HLADR3/4-DQ8 comprise almost 50% of children who develop antiislet autoimmunity by the age of 5 years. Genetic risk for type 1 diabetes can be further stratified by selection of children with susceptible genotypes at other diabetes genes, by selection of children with a multiple family history of diabetes, and/or by selection of relatives that are HLA identical to the proband. SUMMARY: Children with the HLA-risk genotypes DR3/4-DQ8 or DR4/DR4 who have a family history of type 1 diabetes have more than a 1 in 5 risk for developing islet autoantibodies during childhood, and children with the same HLA-risk genotype but no family history have approximately a 1 in 20 risk. Determining extreme genetic risk is a prerequisite for the implementation of primary prevention trials, which are now underway for relatives of individuals with type 1 diabetes.
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Identifiers
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.