ArticleJournal of clinical medicine2016
B Cell Receptor Affinity for Insulin Dictates Autoantigen Acquisition and B Cell Functionality in Autoimmune Diabetes.
Article in Journal of clinical medicine, 2016. 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, 22 citations in OpenAlex.
- Altered B cell metabolic pathways characterize type 1 diabetes progression.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Spatial Changes in Hippocampal Transcriptomic Profiles Following Limbic Non-convulsive Status Epilepticus: Insights into Long-Term Inflammation and Cognitive Deficits.Molecular neurobiology · 2026Article
- Evaluation of proinsulin(F25D) as a targeting ligand for insulin-binding B cells in autoimmune diabetes.Drug delivery and translational research · 2026Article
- POU2F2 activates the Akt/mTOR signalling pathway and enhances B lymphocyte function during diabetic kidney disease by promoting PIK3CD transcription.Nephrology (Carlton, Vic.) · 2024Article
- CD4Immunity · 2024Article
- Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024Review
- Factors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.Antibodies (Basel, Switzerland) · 2024Review
- PLAC8 contributes to the malignant behaviors of cervical cancer cells by activating the SOX4-mediated AKT pathway.Histochemistry and cell biology · 2023Article
- 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
- B Quiet: Autoantigen-Specific Strategies to Silence Raucous B Lymphocytes and Halt Cross-Talk with T Cells in Type 1 Diabetes.Biomedicines · 2021Review
- Revisiting the Antigen-Presenting Function of β Cells in T1D Pathogenesis.Frontiers in immunology · 2021Review
- High-Dose IV Administration of Rasburicase Suppresses Anti-rasburicase Antibodies, Depletes Rasburicase-Specific Lymphocytes, and Upregulates Treg Cells.The AAPS journal · 2020Article
- B cell tolerance and antibody production to the celiac disease autoantigen transglutaminase 2.The Journal of experimental medicine · 2020Article
- Generation of T Cell Receptor Retrogenic Mice.Current protocols in immunology · 2019Article
- B-Lymphocyte Phenotype Determines T-Lymphocyte Subset Differentiation in Autoimmune Diabetes.Frontiers in immunology · 2019Article
- Silencing of high-affinity insulin-reactive B lymphocytes by anergy and impact of the NOD genetic background in mice.Diabetologia · 2018Article
- B cells in type 1 diabetes mellitus and diabetic kidney disease.Nature reviews. Nephrology · 2017Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
B cells have been strongly implicated in the development of human type 1 diabetes and are required for disease in the NOD mouse model. These functions are dependent on B cell antigen receptor (BCR) specificity and expression of MHC, implicating linked autoantigen recognition and presentation to effector T cells. BCR-antigen affinity requirements for participation in disease are unclear. We hypothesized that BCR affinity for the autoantigen insulin differentially affects lymphocyte functionality, including tolerance modality and the ability to acquire and become activated in the diabetogenic environment. Using combined transgenic and retrogenic heavy and light chain to create multiple insulin-binding BCRs, we demonstrate that affinity for insulin is a critical determinant of the function of these autoreactive cells. We show that both BCR affinity for insulin and genetic background affect tolerance induction in immature B cells. We also find new evidence that may explain the enigmatic ability of B cells expressing 125 anti-insulin BCR to support development of TID in NOD mice despite a reported affinity beneath requirements for binding insulin at in vivo concentrations. We report that when expressed as an antigen receptor the affinity of 125 is much higher than determined by measurements of the soluble form. Finally, we show that in vivo acquisition of insulin requires both sufficient BCR affinity and permissive host/tissue environment. We propose that a confluence of BCR affinity, pancreas environment, and B cell tolerance-regulating genes in the NOD animal allows acquisition of insulin and autoimmunity.
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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.