ReviewImmunology and cell biology2021
De-coding genetic risk variants in type 1 diabetes.
Review in Immunology and cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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.
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Who cites it
31 citing papers in PubMed.
- ProtectiveiScience · 2026Article
- Genetic and molecular evidence linking CTSH to Alzheimer's disease pathophysiology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Type I Interferons as Contextual Regulators of B-Cell Tolerance in Type 1 Diabetes.Biomolecules · 2026Review
- Research progress and application prospects of multi-omics integration strategies in precision risk stratification of type 1 diabetes mellitus.Frontiers in immunology · 2026Review
- Imbalance of stem-like and effector T cell states in children with early type 1 diabetes across conventional and regulatory subsets.Nature communications · 2025Article
- Proteogenomic Discovery of Novel Open Reading Frames With HLA Immune Presentation on Human β-Cells.Diabetes · 2025Article
- Reduced Function of the Adaptor SH2B3 Promotes T1D via Altered Cytokine-Regulated, T-Cell-Intrinsic Immune Tolerance.Diabetes · 2025Article
- Immune perturbations in human pancreas lymphatic tissues prior to and after type 1 diabetes onset.Nature communications · 2025Article
- Inhibition of CD226 co-stimulation suppresses diabetes development in the NOD mouse by augmenting regulatory T cells and diminishing effector T cell function.Diabetologia · 2025Article
- Linking epigenetic mechanisms of T cell dysfunction with pathophysiology of type 1 diabetes mellitus.Frontiers in immunology · 2025Review
- The perfect storm: unraveling the interplay of genetic predisposition and viral triggers in type 1 diabetes pathogenesis.Frontiers in endocrinology · 2025Review
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Inhibition of CD226 Co-Stimulation Suppresses Diabetes Development in the NOD Mouse by Augmenting Tregs and Diminishing Effector T Cell Function.bioRxiv : the preprint server for biology · 2024Article
- Investigation of missense mutation-related type 1 diabetes mellitus through integrating genomic databases and bioinformatic approach.Genomics & informatics · 2024Article
- Genetic and Epigenetic Aspects of Type 1 Diabetes Mellitus: Modern View on the Problem.Biomedicines · 2024Review
- Identification of functional enhancer variants associated with type I diabetes in CD4+ T cells.Frontiers in immunology · 2024Article
- Gene-environment interaction in the pathophysiology of type 1 diabetes.Frontiers in endocrinology · 2024Article
- Treg-Specific CD226 Deletion Reduces Diabetes Incidence in NOD Mice by Improving Regulatory T-Cell Stability.Diabetes · 2023Article
- Insulin-like Growth Factor-1 Synergizes with IL-2 to Induce Homeostatic Proliferation of Regulatory T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- TheInternational journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The conceptual basis for a genetic predisposition underlying the risk for developing type 1 diabetes (T1D) predates modern human molecular genetics. Over half of the genetic risk has been attributed to the human leukocyte antigen (HLA) class II gene region and to the insulin (INS) gene locus - both thought to confer direction of autoreactivity and tissue specificity. Notwithstanding, questions still remain regarding the functional contributions of a vast array of minor polygenic risk variants scattered throughout the genome that likely influence disease heterogeneity and clinical outcomes. Herein, we summarize the available literature related to the T1D-associated coding variants defined at the time of this review, for the genes PTPN22, IFIH1, SH2B3, CD226, TYK2, FUT2, SIRPG, CTLA4, CTSH and UBASH3A. Data from genotype-selected human cohorts are summarized, and studies from the non-obese diabetic (NOD) mouse are presented to describe the functional impact of these variants in relation to innate and adaptive immunity as well as to β-cell fragility, with expression profiles in tissues and peripheral blood highlighted. The contribution of each variant to progression through T1D staging, including environmental interactions, are discussed with consideration of how their respective protein products may serve as attractive targets for precision medicine-based therapeutics to prevent or suspend the development of T1D.
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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.