ArticleDiabetes2009
Activation of insulin-reactive CD8 T-cells for development of autoimmune diabetes.
Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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Who cites it
42 citing papers in PubMed, 73 citations in OpenAlex.
- Proinsulin-Loaded Nanoparticles Suppress Insulitis and Induce Temporary Diabetes Remission.Cells · 2026Article
- Imbalance of T cell subsets: a core event that mediates the progression of T2DM and its complications.Frontiers in immunology · 2025Review
- Androgens contribute to sex bias of autoimmunity in mice by T cell-intrinsic regulation of Ptpn22 phosphatase expression.Nature communications · 2024Article
- Regulatory CD4Frontiers in immunology · 2024Article
- Insulin-degrading enzyme regulates insulin-directed cellular autoimmunity in murine type 1 diabetes.Frontiers in immunology · 2024Article
- Islet-specific CD8Immunology and cell biology · 2023Article
- Novel engineered B lymphocytes targeting islet-specific T cells inhibit the development of type 1 diabetes in non-obese diabetic Scid mice.Frontiers in immunology · 2023Article
- A gut microbial peptide and molecular mimicry in the pathogenesis of type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Insulin B-chain hybrid peptides are agonists for T cells reactive to insulin B:9-23 in autoimmune diabetes.Frontiers in immunology · 2022Article
- Short Duration Alagebrium Chloride Therapy Prediabetes Does Not Inhibit Progression to Autoimmune Diabetes in an Experimental Model.Metabolites · 2021Article
- Differentiating MHC-Dependent and -Independent Mechanisms of Lymph Node Stromal Cell Regulation of Proinsulin-Specific CD8Diabetes · 2021Article
- Drug-Integrating Amphiphilic Nanomaterial Assemblies: 1. Spatiotemporal control of cyclosporine delivery and activity using nanomicelles and nanofibrils.Journal of controlled release : official journal of the Controlled Release Society · 2021Article
- Presumption of guilt for T cells in type 1 diabetes: lead culprits or partners in crime depending on age of onset?Diabetologia · 2021Review
- Oral Fc-Coupled Preproinsulin Achieves Systemic and Thymic Delivery Through the Neonatal Fc Receptor and Partially Delays Autoimmune Diabetes.Frontiers in immunology · 2021Article
- Tolerance to Proinsulin-1 Reduces Autoimmune Diabetes in NOD Mice.Frontiers in immunology · 2021Article
- Dendritic cells license regulatory B cells to produce IL-10 and mediate suppression of antigen-specific CD8 T cells.Cellular & molecular immunology · 2020Article
- Phenotypically distinct anti-insulin B cells repopulate pancreatic islets after anti-CD20 treatment in NOD mice.Diabetologia · 2019Article
- Article
- eIF5A inhibition influences T cell dynamics in the pancreatic microenvironment of the humanized mouse model of Type 1 Diabetes.Scientific reports · 2019Article
- Self-Transducible Bimodal PDX1-FOXP3 Protein Lifts Insulin Secretion and Curbs Autoimmunity, Boosting Tregs in Type 1 Diabetic Mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
objectiveWe have previously reported a highly diabetogenic CD8 T-cell clone, G9C8, in the nonobese diabetic (NOD) mouse, specific to low-avidity insulin peptide B15-23, and cells responsive to this antigen are among the earliest islet infiltrates. We aimed to study the selection, activation, and development of the diabetogenic capacity of these insulin-reactive T-cells. RESEARCH DESIGN AND
methodsWe generated a T-cell receptor (TCR) transgenic mouse expressing the cloned TCR Valpha18/Vbeta6 receptor of the G9C8 insulin-reactive CD8 T-cell clone. The mice were crossed to TCRCalpha-/- mice so that the majority of the T-cells expressed the clonotypic TCR, and the phenotype and function of the cells was investigated.
resultsThere was good selection of CD8 T-cells with a predominance of CD8 single-positive thymocytes, in spite of thymic insulin expression. Peripheral lymph node T-cells had a naïve phenotype (CD44lo, CD62Lhi) and proliferated to insulin B15-23 peptide and to insulin. These cells produced interferon-gamma and tumor necrosis factor-alpha in response to insulin peptide and were cytotoxic to insulin peptide-coated targets. In vivo, the TCR transgenic mice developed insulitis but not spontaneous diabetes. However, the mice developed diabetes on immunization, and the activated transgenic T-cells were able to transfer diabetes to immunodeficient NOD.scid mice.
conclusionsAutoimmune CD8 T-cells responding to a low-affinity insulin B-chain peptide escape from thymic negative selection and require activation in vivo to cause diabetes.
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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.