ArticleDiabetes2012
Germline TRAV5D-4 T-cell receptor sequence targets a primary insulin peptide of NOD mice.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- Quantitative V gene-targeted T cell receptor sequencing as a biomarker in type 1 diabetes.JCI insight · 2026Article
- Identification of Sjögren's disease-associated T cell receptor motifs through deep sequencing.JCI insight · 2025Article
- CD4Immunity · 2024Article
- Aire mediates tolerance to insulin through thymic trimming of high-affinity T cell clones.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Activation pathways that drive CD4Immunological reviews · 2022Review
- Autoreactive T cell receptors with shared germline-like α chains in type 1 diabetes.JCI insight · 2021Article
- T Cell Receptor Genotype andGenes · 2021Article
- Using the T Cell Receptor as a Biomarker in Type 1 Diabetes.Frontiers in immunology · 2021Review
- Combining Well-Tempered Metadynamics Simulation and SPR Assays to Characterize the Binding Mechanism of the Universal T-Lymphocyte Tetanus Toxin Epitope TT830-843.BioMed research international · 2021Article
- How C-terminal additions to insulin B-chain fragments create superagonists for T cells in mouse and human type 1 diabetes.Science immunology · 2019Article
- TCR Retrogenic Mice as a Model To Map Self-Tolerance Mechanisms to the Cancer Mucosa Antigen GUCY2C.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Development of T cell lines sensitive to antigen stimulation.Journal of immunological methods · 2018Article
- Simultaneous Recognition of Allogeneic MHC and Cognate Autoantigen by Autoreactive T Cells in Transplant Rejection.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- C-terminal modification of the insulin B:11-23 peptide creates superagonists in mouse and human type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Tissue distribution and clonal diversity of the T and B cell repertoire in type 1 diabetes.JCI insight · 2016Article
- Molecular Interactions Governing Autoantigen Presentation in Type 1 Diabetes.Current diabetes reports · 2015Review
- Prediction and prevention of type 1 diabetes: update on success of prediction and struggles at prevention.Pediatric diabetes · 2015Review
- N-terminal additions to the WE14 peptide of chromogranin A create strong autoantigen agonists in type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Monoclonal antibody blocking the recognition of an insulin peptide-MHC complex modulates type 1 diabetes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Autoantigen-induced focusing of Vβ13+ T cells precedes onset of autoimmune diabetes in the LEW.1WR1 rat.Diabetes · 2014Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
There is accumulating evidence that autoimmunity to insulin B chain peptide, amino acids 9-23 (insulin B:9-23), is central to development of autoimmune diabetes of the NOD mouse model. We hypothesized that enhanced susceptibility to autoimmune diabetes is the result of targeting of insulin by a T-cell receptor (TCR) sequence commonly encoded in the germline. In this study, we aimed to demonstrate that a particular Vα gene TRAV5D-4 with multiple junction sequences is sufficient to induce anti-islet autoimmunity by studying retrogenic mouse lines expressing α-chains with different Vα TRAV genes. Retrogenic NOD strains expressing Vα TRAV5D-4 α-chains with many different complementarity determining region (CDR) 3 sequences, even those derived from TCRs recognizing islet-irrelevant molecules, developed anti-insulin autoimmunity. Induction of insulin autoantibodies by TRAV5D-4 α-chains was abrogated by the mutation of insulin peptide B:9-23 or that of two amino acid residues in CDR1 and 2 of the TRAV5D-4. TRAV13-1, the human ortholog of murine TRAV5D-4, was also capable of inducing in vivo anti-insulin autoimmunity when combined with different murine CDR3 sequences. Targeting primary autoantigenic peptides by simple germline-encoded TCR motifs may underlie enhanced susceptibility to the development of autoimmune diabetes.
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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.