ArticleScience (New York, N.Y.)2016
Pathogenic CD4 T cells in type 1 diabetes recognize epitopes formed by peptide fusion.
Article in Science (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 342 papers.
What it found
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Who cites it
342 citing papers in PubMed, 486 citations in OpenAlex.
- Increasing plasma glucose before the development of type 1 diabetes-the TRIGR study.Pediatric diabetes · 2021Trial
- Discovery of Post-Translationally Modified Epitopes in Autoimmunity: Someone Has to Fish so Everyone Can Eat.Immunological reviews · 2026Review
- Oxidative Stress, Post-Translational Modifications, and Type 1 Diabetes Pathogenesis.Immunological reviews · 2026Review
- Beta Cell Stress to Epitope Diversification: Post-Translationally Modified Antigens in Type 1 Diabetes.Immunological reviews · 2026Review
- B Lymphocytes in Latent Autoimmune Diabetes in Adults: From Autoimmune Activation to Immunometabolic Heterogeneity and Precision Therapeutic Perspectives.Diabetes/metabolism research and reviews · 2026Review
- From Disposal to Display: Crinophagy as a β-Cell Source of Neoantigens in Type 1 Diabetes.Immunological reviews · 2026Review
- Citrullination and Deamidation in Type 1 Diabetes: Linking Beta Cell Stress to Neoantigen-Driven Autoimmunity.Immunological reviews · 2026Review
- Oxidative Post-Translational Modifications of Insulin in Type 1 Diabetes Autoimmunity.Immunological reviews · 2026Review
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- Hybrid Insulin Peptides as Antigens and Tolerogens for Pathogenic T Cells in Autoimmune Diabetes.Immunological reviews · 2026Review
- Personalized cancer vaccines: bridging immune-oncology and precision medicine for advanced therapeutics.Signal transduction and targeted therapy · 2026Review
- Unbiased discovery of autoreactive type 1 diabetes T-cell receptors that bind specific hybrid insulin peptides.Research square · 2026Article
- Murine and Humanized Mouse Models in Autoimmune Disease Research and Therapeutics Development.Biology · 2026Review
- Crinophagy in Pancreatic Beta Cells: From Insulin Granule Turnover to Diabetes Pathogenesis.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Multi-tissue multi-omics integration reveals tissue-specific pathways, gene networks and drug candidates for type 1 diabetes.Diabetologia · 2026Article
- Beta cell reactivity defines disease-relevant pancreatic CD8 T cells in type 1 diabetes.bioRxiv : the preprint server for biology · 2026Article
- New and emerging therapies in type 1 diabetes mellitus.The Journal of clinical investigation · 2026Review
- TOX drives CD4Nature immunology · 2026Article
- Emerging therapies for type 1 diabetes: Immunotherapy and gene editing advances.The Journal of international medical research · 2026Review
- Islet amyloid disrupts MHC class II antigen presentation and delays autoimmune diabetes in NOD mice.Diabetologia · 2026Article
282 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
T cell-mediated destruction of insulin-producing β cells in the pancreas causes type 1 diabetes (T1D). CD4 T cell responses play a central role in β cell destruction, but the identity of the epitopes recognized by pathogenic CD4 T cells remains unknown. We found that diabetes-inducing CD4 T cell clones isolated from nonobese diabetic mice recognize epitopes formed by covalent cross-linking of proinsulin peptides to other peptides present in β cell secretory granules. These hybrid insulin peptides (HIPs) are antigenic for CD4 T cells and can be detected by mass spectrometry in β cells. CD4 T cells from the residual pancreatic islets of two organ donors who had T1D also recognize HIPs. Autoreactive T cells targeting hybrid peptides may explain how immune tolerance is broken in T1D.
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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.