ArticleThe Journal of clinical investigation2007
Priming and effector dependence on insulin B:9-23 peptide in NOD islet autoimmunity.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 107 citations in OpenAlex.
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- Quantitative V gene-targeted T cell receptor sequencing as a biomarker in type 1 diabetes.JCI insight · 2026Article
- Submicron-sized ultrasound contrast agents as therapeutic peptide delivery vehicles in type 1 diabetes.Theranostics · 2026Article
- Review
- Oral tolerogenic vaccine combined with gastrin restores immune tolerance and beta-cell function in NOD mice with Type 1 diabetes.Frontiers in immunology · 2025Article
- Autoimmune diseases: targets, biology, and drug discovery.Acta pharmacologica Sinica · 2024Review
- Mechanism of Action of OralVaccines · 2024Article
- Mechanistic Insights into Immune-Microbiota Interactions and Preventive Role of Probiotics Against Autoimmune Diabetes Mellitus.Probiotics and antimicrobial proteins · 2023Review
- Using mass spectrometry to identify neoantigens in autoimmune diseases: The type 1 diabetes example.Seminars in immunology · 2023Review
- MHC Class II Presentation in Autoimmunity.Cells · 2023Review
- Changes in the gut microbiota of NOD mice in response to an oral Salmonella-based vaccine against type 1 diabetes.PloS one · 2023Article
- The good and the bad of T cell cross-reactivity: challenges and opportunities for novel therapeutics in autoimmunity and cancer.Frontiers in immunology · 2023Review
- Blood leukocytes recapitulate diabetogenic peptide-MHC-II complexes displayed in the pancreatic islets.The Journal of experimental medicine · 2021Article
- T-cell responses to hybrid insulin peptides prior to type 1 diabetes development.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Therapeutic Targeting of Autoreactive B Cells: Why, How, and When?Biomedicines · 2021Review
- Immunoregulatory Effect ofDrug design, development and therapy · 2021Article
- Tolerance to Proinsulin-1 Reduces Autoimmune Diabetes in NOD Mice.Frontiers in immunology · 2021Article
- Exploring the Triple Interaction between the Host Genome, the Epigenome, and the Gut Microbiome in Type 1 Diabetes.International journal of molecular sciences · 2020Review
- Retro-inverso D-peptides as a novel targeted immunotherapy for Type 1 diabetes.Journal of autoimmunity · 2020Article
- Cepharanthine blocks TSH receptor peptide presentation by HLA-DR3: Therapeutic implications to Graves' disease.Journal of autoimmunity · 2020Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
NOD mice with knockout of both native insulin genes and a mutated proinsulin transgene, alanine at position B16 in preproinsulin (B16:A-dKO mice), do not develop diabetes. Transplantation of NOD islets, but not bone marrow, expressing native insulin sequences (tyrosine at position B16) into B16:A-dKO mice rapidly restored development of insulin autoantibodies (IAAs) and insulitis, despite the recipients' pancreatic islets lacking native insulin sequences. Splenocytes from B16:A-dKO mice that received native insulin-positive islets induced diabetes when transferred into wild-type NOD/SCID or B16:A-dKO NOD/SCID mice. Splenocytes from mice immunized with native insulin B chain amino acids 9-23 (insulin B:9-23) peptide in CFA induced rapid diabetes upon transfer only in recipients expressing the native insulin B:9-23 sequence in their pancreata. Additionally, CD4(+) T cells from B16:A-dKO mice immunized with native insulin B:9-23 peptide promoted IAAs in NOD/SCID mice. These results indicate that the provision of native insulin B:9-23 sequences is sufficient to prime anti-insulin autoimmunity and that subsequent transfer of diabetes following peptide immunization requires native insulin B:9-23 expression in islets. Our findings demonstrate dependence on B16 alanine versus tyrosine of insulin B:9-23 for both the initial priming and the effector phase of NOD anti-islet autoimmunity.
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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.