ArticleDiabetes2011
Anti-islet autoantibodies trigger autoimmune diabetes in the presence of an increased frequency of islet-reactive CD4 T cells.
Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 72 citations in OpenAlex.
- Weighted Gene Coexpression Network Analysis Identified MicroRNA Coexpression Modules and Related Pathways in Type 2 Diabetes Mellitus.Oxidative medicine and cellular longevity · 2019Trial
- Diurnal Variation of Islet Autoantibody Titers in Established Type 1 Diabetes Suggests Restricted-Time Sampling Improves Aab Measurement and Detection.Research square · 2026Article
- Activated polyreactive B cells are clonally expanded in autoantibody positive and patients with recent-onset type 1 diabetes.Cell reports · 2025Article
- Review
- Islet-antigen reactive B cells display a unique phenotype and BCR repertoire in autoantibody positive and recent-onset type 1 diabetes patients.bioRxiv : the preprint server for biology · 2024Article
- Non-coding autoimmune risk variant defines role for ICOS in T peripheral helper cell development.Nature communications · 2024Article
- The role of B cells in the pathogenesis of type 1 diabetes.Frontiers in immunology · 2024Review
- Cancer-Derived Immunoglobulin G and Pancreatic Cancer.Advances in experimental medicine and biology · 2024Review
- The Expression of Non B Cell-Derived Immunoglobulins.Advances in experimental medicine and biology · 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
- Activation pathways that drive CD4Immunological reviews · 2022Review
- Evidence of genetic epistasis in autoimmune diabetes susceptibility revealed by mouse congenic sublines.Immunogenetics · 2021Article
- Epigenetic Changes Induced by Maternal Factors during Fetal Life: Implication for Type 1 Diabetes.Genes · 2021Review
- Emerging Roles of Myeloid-Derived Suppressor Cells in Diabetes.Frontiers in pharmacology · 2021Review
- The Multiple Roles of B Lymphocytes in the Onset and Treatment of Type 1 Diabetes: Interactions between B Lymphocytes and T Cells.Journal of diabetes research · 2021Review
- T-B Lymphocyte Interactions Promote Type 1 Diabetes Independently of SLAM-Associated Protein.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Mesenchymal stromal cell therapies: immunomodulatory properties and clinical progress.Stem cell research & therapy · 2020Review
- Microbiota-derived butyrate limits the autoimmune response by promoting the differentiation of follicular regulatory T cells.EBioMedicine · 2020Article
- Type 1 diabetes pathogenesis and the role of inhibitory receptors in islet tolerance.Annals of the New York Academy of Sciences · 2020Review
- Role of the PD-1/PD-L1 Dyad in the Maintenance of Pancreatic Immune Tolerance for Prevention of Type 1 Diabetes.Frontiers in endocrinology · 2020Review
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo define cellular mechanisms by which B cells promote type 1 diabetes. RESEARCH DESIGN AND
methodsThe study measured islet-specific CD4 T cell regulation in T-cell receptor transgenic mice with elevated frequencies of CD4 T cells recognizing hen egg lysozyme (HEL) autoantigen expressed in islet β-cells and thymic epithelium under control of the insulin-gene promoter. The effects of a mutation in Roquin that dysregulates T follicular helper (Tfh) cells to promote B-cell activation and anti-islet autoantibodies were studied, as were the effects of HEL antigen-presenting B cells and passively transferred or maternally transmitted anti-islet HEL antibodies.
resultsMouse anti-islet IgG antibodies-either formed as a consequence of excessive Tfh activity, maternally transmitted, or passively transferred-caused a breakdown of tolerance in islet-reactive CD4(+) cells and fast progression to diabetes. Progression to diabetes was ameliorated in the absence of B cells or when the B cells could not secrete islet-specific IgG. Anti-islet antibodies increased the survival of proliferating islet-reactive CD4(+) T cells. FcγR blockade delayed and reduced the incidence of autoimmune diabetes.
conclusionsB cells can promote type 1 diabetes by secreting anti-islet autoantibodies that act in an FcγR-mediated manner to enhance the expansion of islet-reactive CD4 T cells and cooperate with inherited defects in thymic and peripheral CD4 T-cell tolerance. Cooperation between inherited variants affecting CD4 T-cell tolerance and anti-islet autoantibodies should be examined in epidemiological studies and in studies examining the efficacy of B-cell depletion.
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