ArticleJournal of immunology (Baltimore, Md. : 1950)2013
B lymphocyte "original sin" in the bone marrow enhances islet autoreactivity in type 1 diabetes-prone nonobese diabetic mice.
Article in Journal of immunology (Baltimore, Md. : 1950), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 33 citations in OpenAlex.
- Dual Modulation of Prostaglandin E2 Receptors EP3 and EP4 Protects β-Cell Mass in a Model of Aggressive Autoimmune Inflammation.Diabetes · 2026Article
- BCL6 in T cells promotes type 1 diabetes by redirecting fates of insulin-autoreactive B lymphocytes.iScience · 2026Article
- Altered B cell metabolic pathways characterize type 1 diabetes progression.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Article
- Factors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.Antibodies (Basel, Switzerland) · 2024Review
- CD22L Conjugation to Insulin Attenuates Insulin-Specific B Cell Activation.Bioconjugate chemistry · 2023Article
- Productive Germinal Center Responses Depend on the Nature of Stimuli Received by Anti-Insulin B Cells in Type 1 Diabetes-Prone Mice.ImmunoHorizons · 2023Article
- Comparative analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone and resistant mice.Frontiers in immunology · 2022Article
- B Quiet: Autoantigen-Specific Strategies to Silence Raucous B Lymphocytes and Halt Cross-Talk with T Cells in Type 1 Diabetes.Biomedicines · 2021Review
- T-B Lymphocyte Interactions Promote Type 1 Diabetes Independently of SLAM-Associated Protein.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Single-cell RNA sequencing of murine islets shows high cellular complexity at all stages of autoimmune diabetes.The Journal of experimental medicine · 2020Article
- Type 1 diabetes pathogenesis and the role of inhibitory receptors in islet tolerance.Annals of the New York Academy of Sciences · 2020Review
- Phenotypically distinct anti-insulin B cells repopulate pancreatic islets after anti-CD20 treatment in NOD mice.Diabetologia · 2019Article
- Silencing of high-affinity insulin-reactive B lymphocytes by anergy and impact of the NOD genetic background in mice.Diabetologia · 2018Article
- Anti-Insulin B Cells Are Poised for Antigen Presentation in Type 1 Diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Genetic and Small Molecule Disruption of the AID/RAD51 Axis Similarly Protects Nonobese Diabetic Mice from Type 1 Diabetes through Expansion of Regulatory B Lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017Review
- B Cell Receptor Affinity for Insulin Dictates Autoantigen Acquisition and B Cell Functionality in Autoimmune Diabetes.Journal of clinical medicine · 2016Article
- Class-switched anti-insulin antibodies originate from unconventional antigen presentation in multiple lymphoid sites.The Journal of experimental medicine · 2016Article
- Genetic, Cellular and Clinical Features of ICF Syndrome: a French National Survey.Journal of clinical immunology · 2016Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Effective central tolerance is required to control the large extent of autoreactivity normally present in the developing B cell repertoire. Insulin-reactive B cells are required for type 1 diabetes in the NOD mouse, because engineered mice lacking this population are protected from disease. The Cg-Tg(Igh-6/Igh-V125)2Jwt/JwtJ (VH125Tg) model is used to define this population, which is found with increased frequency in the periphery of NOD mice versus nonautoimmune C57BL/6 VH125Tg mice; however, the ontogeny of this disparity is unknown. To better understand the origins of these pernicious B cells, anti-insulin B cells were tracked during development in the polyclonal repertoire of VH125Tg mice. An increased proportion of insulin-binding B cells is apparent in NOD mice at the earliest point of Ag commitment in the bone marrow. Two predominant L chains were identified in B cells that bind heterologous insulin. Interestingly, Vκ4-57-1 polymorphisms that confer a CDR3 Pro-Pro motif enhance self-reactivity in VH125Tg/NOD mice. Despite binding circulating autoantigen in vivo, anti-insulin B cells transition from the parenchyma to the sinusoids in the bone marrow of NOD mice and enter the periphery unimpeded. Anti-insulin B cells expand at the site of autoimmune attack in the pancreas and correlate with increased numbers of IFN-γ-producing cells in the repertoire. These data identify the failure to cull autoreactive B cells in the bone marrow as the primary source of anti-insulin B cells in NOD mice and suggest that dysregulation of central tolerance permits their escape into the periphery to promote disease.
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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.