ArticleJournal of immunology (Baltimore, Md. : 1950)2018
HLA-B*39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression.
Article in Journal of immunology (Baltimore, Md. : 1950), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Sex as a modifier of genetic risk for type 1 diabetes.Diabetes, obesity & metabolism · 2025Review
- Humanized Mouse Models for Type 1 Diabetes.Current protocols · 2025Review
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- 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
- Viruses as a potential environmental trigger of type 1 diabetes mellitus (Review).Biomedical reports · 2024Review
- Fifty years of HLA-associated type 1 diabetes risk: history, current knowledge, and future directions.Frontiers in immunology · 2024Review
- Next-generation sequencing reveals additional HLA class I and class II alleles associated with type 1 diabetes and age at onset.Frontiers in immunology · 2024Article
- HLA-B*13, B*35 and B*39 Alleles Are Closely Associated With the Lack of Response to ART in HIV Infection: A Cohort Study in a Population of Northern Brazil.Frontiers in immunology · 2022Article
- Preclinical Models to Evaluate the Human Response to Autoantigen and Antigen-Specific Immunotherapy in Human Type 1 Diabetes.Frontiers in endocrinology · 2022Review
- Genetic Modifiers of Thymic Selection and Central Tolerance in Type 1 Diabetes.Frontiers in immunology · 2022Review
- A Humanized Mouse Strain That Develops Spontaneously Immune-Mediated Diabetes.Frontiers in immunology · 2021Article
- New Insights into the Genetics of Latent Autoimmune Diabetes in Adults.Current diabetes reports · 2020Review
- Genetic Discrimination Between LADA and Childhood-Onset Type 1 Diabetes Within the MHC.Diabetes care · 2020Article
- Model validity for preclinical studies in precision medicine: precisely how precise do we need to be?Mammalian genome : official journal of the International Mammalian Genome Society · 2019Article
- The Evolving Landscape of Autoantigen Discovery and Characterization in Type 1 Diabetes.Diabetes · 2019Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Type 1 diabetes (T1D) is characterized by T cell-mediated destruction of the insulin-producing β cells of the pancreatic islets. Among the loci associated with T1D risk, those most predisposing are found in the MHC region. HLA-B*39:06 is the most predisposing class I MHC allele and is associated with an early age of onset. To establish an NOD mouse model for the study of HLA-B*39:06, we expressed it in the absence of murine class I MHC. HLA-B*39:06 was able to mediate the development of CD8 T cells, support lymphocytic infiltration of the islets, and confer T1D susceptibility. Because reduced thymic insulin expression is associated with impaired immunological tolerance to insulin and increased T1D risk in patients, we incorporated this in our model as well, finding that HLA-B*39:06-transgenic NOD mice with reduced thymic insulin expression have an earlier age of disease onset and a higher overall prevalence as compared with littermates with typical thymic insulin expression. This was despite virtually indistinguishable blood insulin levels, T cell subset percentages, and TCR Vβ family usage, confirming that reduced thymic insulin expression does not impact T cell development on a global scale. Rather, it will facilitate the thymic escape of insulin-reactive HLA-B*39:06-restricted T cells, which participate in β cell destruction. We also found that in mice expressing either HLA-B*39:06 or HLA-A*02:01 in the absence of murine class I MHC, HLA transgene identity alters TCR Vβ usage by CD8 T cells, demonstrating that some TCR Vβ families have a preference for particular class I MHC alleles.
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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.