ArticleDiabetologia2018
Silencing of high-affinity insulin-reactive B lymphocytes by anergy and impact of the NOD genetic background in mice.
Article in Diabetologia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Lyn governs the establishment and maintenance of B cell anergy by suppressing PI3K signaling.Nature communications · 2026Article
- Evaluation of proinsulin(F25D) as a targeting ligand for insulin-binding B cells in autoimmune diabetes.Drug delivery and translational research · 2026Article
- Deletion of Ptpn2 in B cells promotes autoimmunity via TLR and JAK/STAT signaling.JCI insight · 2025Article
- Factors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.Antibodies (Basel, Switzerland) · 2024Review
- Identification of an anergic BND cell-derived activated B cell population (BND2) in young-onset type 1 diabetes patients.The Journal of experimental medicine · 2023Article
- Role of inhibitory signaling in peripheral B cell tolerance.Immunological reviews · 2022Review
- Increased plasmablasts enhance T cell-mediated beta cell destruction and promote the development of type 1 diabetes.Molecular medicine (Cambridge, Mass.) · 2022Article
- Polygenic autoimmune disease risk alleles impacting B cell tolerance act in concert across shared molecular networks in mouse and in humans.Frontiers in immunology · 2022Review
- Comparative analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone and resistant mice.Frontiers in immunology · 2022Article
- Enrichment and Detection of Antigen-Binding B Cells for Mass Cytometry.Magnetochemistry (Basel, Switzerland) · 2021Article
- Article
- B Quiet: Autoantigen-Specific Strategies to Silence Raucous B Lymphocytes and Halt Cross-Talk with T Cells in Type 1 Diabetes.Biomedicines · 2021Review
- Tetrameric Fluorescent Antigen Arrays for Single-Step Identification of Antigen-Specific B Cells.Journal of visualized experiments : JoVE · 2020Article
- Endotypes in T1D: B lymphocytes and early onset.Current opinion in endocrinology, diabetes, and obesity · 2020Review
- Phenotypically distinct anti-insulin B cells repopulate pancreatic islets after anti-CD20 treatment in NOD mice.Diabetologia · 2019Article
- Non-Antibody-Secreting Functions of B Cells and Their Contribution to Autoimmune Disease.Annual review of cell and developmental biology · 2019Review
- A Precision B Cell-Targeted Therapeutic Approach to Autoimmunity Caused by Phosphatidylinositol 3-Kinase Pathway Dysregulation.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Techniques to Study Antigen-Specific B Cell Responses.Frontiers in immunology · 2019Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
aims/hypothesisPrevious studies have demonstrated that high-affinity insulin-binding B cells (IBCs) silenced by anergy in healthy humans lose their anergy in islet autoantibody-positive individuals with recent-onset type 1 diabetes, and in autoantibody-negative first-degree relatives carrying certain risk alleles. Here we explore the hypothesis that IBCs are found in the immune periphery of disease-resistant C57BL/6-H2g7 mice, where, as in healthy humans, they are anergic, but that in disease-prone genetic backgrounds (NOD) they become activated and migrate to the pancreas and pancreatic lymph nodes, where they participate in the development of type 1 diabetes.
methodsWe compared the status of high-affinity IBCs in disease-resistant VH125.C57BL/6-H2g7 and disease-prone VH125.NOD mice.
resultsConsistent with findings in healthy humans, high-affinity IBCs reach the periphery in disease-resistant mice and are anergic, as indicated by a reduced expression of membrane IgM, unresponsiveness to antigen and failure to become activated or accumulate in the pancreatic lymph nodes or pancreas. In NOD mice, high-affinity IBCs reach the periphery early in life and increase in number prior to the onset of hyperglycaemia. These cells are not anergic; they become activated, produce autoantibodies and accumulate in the pancreas and pancreatic lymph nodes prior to disease development. CONCLUSIONS/
interpretationThese findings are consistent with genetic determination of the escape of high-affinity IBCs from anergy and their early contribution to the development of type 1 diabetes.
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