ArticleJournal of immunology (Baltimore, Md. : 1950)2017
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.
Article in Journal of immunology (Baltimore, Md. : 1950), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
29 citing papers in PubMed, 36 citations in OpenAlex.
- Multi-tissue multi-omics integration reveals tissue-specific pathways, gene networks and drug candidates for type 1 diabetes.Diabetologia · 2026Article
- Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- 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
- Factors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.Antibodies (Basel, Switzerland) · 2024Review
- CD73: agent development potential and its application in diabetes and atherosclerosis.Frontiers in immunology · 2024Review
- The role of B cells in the pathogenesis of type 1 diabetes.Frontiers in immunology · 2024Review
- Applications of Genome-Editing Technologies for Type 1 Diabetes.International journal of molecular sciences · 2023Review
- HLA-DQ8 Supports Development of Insulitis Mediated by Insulin-Reactive Human TCR-Transgenic T Cells in Nonobese Diabetic Mice.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Article
- Activation-induced cytidine deaminase expression by thymic B cells promotes T-cell tolerance and limits autoimmunity.iScience · 2023Article
- DNA repair defects in cancer and therapeutic opportunities.Genes & development · 2022Review
- Genome Editing Using CRISPR-Cas9 and Autoimmune Diseases: A Comprehensive Review.International journal of molecular sciences · 2022Review
- 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
- Engrafting Horse Immune Cells into Mouse Hosts for the Study of the Acute Equine Immune Responses.Animals : an open access journal from MDPI · 2021Article
- Small Molecule Inhibitors of Activation-Induced Deaminase Decrease Class Switch Recombination in B Cells.ACS pharmacology & translational science · 2021Article
- B Quiet: Autoantigen-Specific Strategies to Silence Raucous B Lymphocytes and Halt Cross-Talk with T Cells in Type 1 Diabetes.Biomedicines · 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
- Regulatory B Cells: Role in Type 1 Diabetes.Frontiers in immunology · 2021Review
- Abrogated AID Function Prolongs Survival and Diminishes Renal Pathology in the BXSB Mouse Model of Systemic Lupus Erythematosus.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
B lymphocytes play a key role in type 1 diabetes (T1D) development by serving as a subset of APCs preferentially supporting the expansion of autoreactive pathogenic T cells. As a result of their pathogenic importance, B lymphocyte-targeted therapies have received considerable interest as potential T1D interventions. Unfortunately, the B lymphocyte-directed T1D interventions tested to date failed to halt β cell demise. IgG autoantibodies marking humans at future risk for T1D indicate that B lymphocytes producing them have undergone the affinity-maturation processes of class switch recombination and, possibly, somatic hypermutation. This study found that CRISPR/Cas9-mediated ablation of the activation-induced cytidine deaminase gene required for class switch recombination/somatic hypermutation induction inhibits T1D development in the NOD mouse model. The activation-induced cytidine deaminase protein induces genome-wide DNA breaks that, if not repaired through RAD51-mediated homologous recombination, result in B lymphocyte death. Treatment with the RAD51 inhibitor 4,4'-diisothiocyanatostilbene-2, 2'-disulfonic acid also strongly inhibited T1D development in NOD mice. The genetic and small molecule-targeting approaches expanded CD73
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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.