ArticleProceedings of the National Academy of Sciences of the United States of America2002
Restricted islet-cell reactive T cell repertoire of early pancreatic islet infiltrates in NOD mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 74 citations in OpenAlex.
- Identification of conserved T cell epitopes and flanking amino acid mutants of endogenous retrovirus Gag antigen in nonobese diabetic mice.ImmunoHorizons · 2025Article
- De novo identification of CD4Nature methods · 2024Article
- Unraveling the Immunopathological Landscape of Celiac Disease: A Comprehensive Review.International journal of molecular sciences · 2023Review
- Activation pathways that drive CD4Immunological reviews · 2022Review
- Endogenous retrovirus Gag antigen and its gene variants are unique autoantigens expressed in the pancreatic islets of non-obese diabetic mice.Immunology letters · 2020Article
- Lifelong CMV infection improves immune defense in old mice by broadening the mobilized TCR repertoire against third-party infection.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Single-cell gene expression reveals a landscape of regulatory T cell phenotypes shaped by the TCR.Nature immunology · 2018Article
- Autoimmune Responses to Exosomes and Candidate Antigens Contribute to Type 1 Diabetes in Non-Obese Diabetic Mice.Current diabetes reports · 2017Review
- CD40-mediated signalling influences trafficking, T-cell receptor expression, and T-cell pathogenesis, in the NOD model of type 1 diabetes.Immunology · 2017Article
- High-throughput sequencing reveals restricted TCR Vβ usage and public TCRβ clonotypes among pancreatic lymph node memory CD4(+) T cells and their involvement in autoimmune diabetes.Molecular immunology · 2016Article
- Mechanisms of diabetic autoimmunity: I--the inductive interface between islets and the immune system at onset of inflammation.Immunologic research · 2016Review
- Immune tolerance. Regulatory T cells generated early in life play a distinct role in maintaining self-tolerance.Science (New York, N.Y.) · 2015Article
- Self-pMHCII complexes are variably expressed in the thymus and periphery independent of mRNA expression but dependent on the activation state of the APCs.Molecular immunology · 2015Article
- Reduction of T cell receptor diversity in NOD mice prevents development of type 1 diabetes but not Sjögren's syndrome.PloS one · 2014Article
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- Mouse liver-specific CD8(+) T-cells encounter their cognate antigen and acquire capacity to destroy target hepatocytes.Journal of autoimmunity · 2013Article
- Type 1 diabetes: translating mechanistic observations into effective clinical outcomes.Nature reviews. Immunology · 2013Review
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- T cell populations in the pancreatic lymph node naturally and consistently expand and contract in NOD mice as disease progresses.Molecular immunology · 2012Article
- On the perils of poor editing: regulation of peptide loading by HLA-DQ and H2-A molecules associated with celiac disease and type 1 diabetes.Expert reviews in molecular medicine · 2012Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms responsible for initiating autoimmune diabetes remain obscure. Here, we describe a method for identifying both the alpha- and beta-chains of the T cell receptor (TCR) from individual pancreatic islet-infiltrating T cells at the earliest stages of disease in nonobese diabetic mice (NOD). Analysis of the TCR repertoire of these early islet infiltrates reveals enrichment for a small subset of TCR sequences. Reconstitution of these TCR in vitro demonstrates that these receptors confer reactivity to islet cells but not to the well characterized autoantigens, glutamic acid decarboxylase (GAD65) and insulin. Thus, autoimmune diabetes in NOD may be initiated by a limited number of antigens distinct from GAD65 and insulin.
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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.