ArticleProceedings of the National Academy of Sciences of the United States of America2003
Evidence for a primary islet autoantigen (preproinsulin 1) for insulitis and diabetes in the nonobese diabetic mouse.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 198 citations in OpenAlex.
- Crinophagic granules in pancreatic β cells contribute to mouse autoimmune diabetes by diversifying pathogenic epitope repertoire.Nature communications · 2024Article
- HLA A*24:02-restricted T cell receptors cross-recognize bacterial and preproinsulin peptides in type 1 diabetes.The Journal of clinical investigation · 2024Article
- Human insulin as both antigen and protector in type 1 diabetes.European journal of immunology · 2024Article
- Why does the immune system destroy pancreatic β-cells but not α-cells in type 1 diabetes?Nature reviews. Endocrinology · 2023Review
- Understanding Insulin in the Age of Precision Medicine and Big Data: Under-Explored Nature of Genomics.Biomolecules · 2023Review
- Amino acid polymorphisms in human histocompatibility leukocyte antigen class II and proinsulin epitope have impacts on type 1 diabetes mellitus induced by immune-checkpoint inhibitors.Frontiers in immunology · 2023Article
- Exploration of Immune Targets for Type 1 Diabetes and Latent Autoimmune Disease Immunotherapy.ImmunoTargets and therapy · 2023Review
- Islet-specific CD8Immunology and cell biology · 2023Article
- β-Cell Cre Expression and Reduced Ins1 Gene Dosage Protect Mice From Type 1 Diabetes.Endocrinology · 2022Article
- Preclinical Models to Evaluate the Human Response to Autoantigen and Antigen-Specific Immunotherapy in Human Type 1 Diabetes.Frontiers in endocrinology · 2022Review
- The dark side of insulin: A primary autoantigen and instrument of self-destruction in type 1 diabetes.Molecular metabolism · 2021Review
- Platelet gene therapy induces robust immune tolerance even in a primed model via peripheral clonal deletion of antigen-specific T cells.Molecular therapy. Nucleic acids · 2021Article
- Tolerance to Proinsulin-1 Reduces Autoimmune Diabetes in NOD Mice.Frontiers in immunology · 2021Article
- Glucose, insulin, insulin receptor subunits α and β in normal and spontaneously diabetic and obese ob/ob and db/db infertile mouse testis and hypophysis.Reproductive biology and endocrinology : RB&E · 2020Article
- Tissue-specific autoimmunity controlled by Aire in thymic and peripheral tolerance mechanisms.International immunology · 2020Article
- Adiponectin receptor fragmentation in mouse models of type 1 and type 2 diabetes.Archives of autoimmune diseases · 2020Article
- The presentation of neuroendocrine self-peptides in the thymus: an essential event for individual life and vertebrate survival.Annals of the New York Academy of Sciences · 2019Review
- Development and Characterization of a Preclinical Model for the Evaluation of CD205-Mediated Antigen Delivery Therapeutics in Type 1 Diabetes.ImmunoHorizons · 2019Article
- Transgenic substitution with Greater Amberjack Seriola dumerili fish insulin 2 in NOD mice reduces beta cell immunogenicity.Scientific reports · 2019Article
- Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
It has been reported that an insulin 2 gene knockout, when bred onto nonobese diabetic (NOD) mice, accelerates diabetes. We produced insulin 1 gene knockout congenic NOD mice. In contrast to insulin 2, diabetes and insulitis were markedly reduced in insulin 1 knockout mice, with decreased and delayed diabetes in heterozygous females and no insulitis and diabetes in most homozygous female mice. Lack of insulitis was found for insulin 1 female homozygous knockout mice at 8, 12, and 37 weeks of age. Despite a lack of insulitis, insulin 1 homozygous knockout mice spontaneously expressed insulin autoantibodies. Administration of insulin peptide B:9-23 of both insulin 1 and 2 to NOD mice induced insulin autoantibodies. Insulin 1 is not the only lymphocytic target of NOD mice. Insulin 1 homozygous knockout islets, when transplanted into recently diabetic wild-type NOD mice, became infiltrated with lymphocytes and only transiently reversed diabetes. These observations indicate that loss of either insulin gene can influence progression to diabetes of NOD mice and suggest that the preproinsulin 1 gene is crucial for the spontaneous development of NOD insulitis and 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.