ArticleDiabetes2016
B-lymphocytes expressing an Ig specificity recognizing the pancreatic ß-cell autoantigen peripherin are potent contributors to type 1 diabetes development in NOD mice.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 19 citations in OpenAlex.
- Dia-B-Ties: B Cells in the Islet-Immune-Cell Interface in T1D.Biomolecules · 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
- Comparative analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone and resistant mice.Frontiers in immunology · 2022Article
- The NOD Mouse Beyond Autoimmune Diabetes.Frontiers in immunology · 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
- Biomarkers and Their Possible Functions in the Intestinal Microenvironment of Chagasic Megacolon: An Overview of the (Neuro)inflammatory Process.Journal of immunology research · 2021Review
- T Cells from NOD-Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Prediabetes Induced by a Single Autoimmune B Cell Clone.Frontiers in immunology · 2020Article
- Mediastinal Lymphadenopathy, Class-Switched Auto-Antibodies and Myocardial Immune-Complexes During Heart Failure in Rodents and Humans.Frontiers in cell and developmental biology · 2020Article
- Non-Antibody-Secreting Functions of B Cells and Their Contribution to Autoimmune Disease.Annual review of cell and developmental biology · 2019Review
- Sex-dependent effects of bisphenol A on type 1 diabetes development in non-obese diabetic (NOD) mice.Archives of toxicology · 2019Article
- B-Lymphocyte Phenotype Determines T-Lymphocyte Subset Differentiation in Autoimmune Diabetes.Frontiers in immunology · 2019Article
- Transient BAFF Blockade Inhibits Type 1 Diabetes Development in Nonobese Diabetic Mice by Enriching Immunoregulatory B Lymphocytes Sensitive to Deletion by Anti-CD20 Cotherapy.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Mechanisms by Which B Cells and Regulatory T Cells Influence Development of Murine Organ-Specific Autoimmune Diseases.Journal of clinical medicine · 2017Review
- Interleukin-21 Drives Proliferation and Differentiation of Porcine Memory B Cells into Antibody Secreting Cells.PloS one · 2017Article
- Article
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 2 countries.
Funding
Abstract
While the autoimmune destruction of pancreatic ß-cells underlying type 1 diabetes (1D) development is ultimately mediated by T-cells in NOD mice and also likely humans, B-lymphocytes play an additional key pathogenic role. It appears expression of plasma membrane bound immunoglobulin (Ig) molecules that efficiently capture ß-cell antigens allows autoreactive B-lymphocytes bypassing normal tolerance induction processes to be the subset of antigen presenting cells most efficiently activating diabetogenic T-cells. NOD mice transgenically expressing Ig molecules recognizing antigens that are (insulin) or not (hen egg lysozyme; HEL) expressed by ß-cells have proven useful in dissecting the developmental basis of diabetogenic B-lymphocytes. However, these transgenic Ig specificities were originally selected for their ability to recognize insulin or HEL as foreign, rather than autoantigens. Thus, we generated and characterized NOD mice transgenically expressing an Ig molecule representative of a large proportion of naturally occurring islet-infiltrating B-lymphocytes in NOD mice recognizing the neuronal antigen peripherin. Transgenic peripherin autoreactive B-lymphocytes infiltrate NOD pancreatic islets, acquire an activated proliferative phenotype, and potently support accelerated T1D development. These results support the concept of neuronal autoimmunity as a pathogenic feature of T1D, and targeting such responses could ultimately provide an effective disease intervention approach.
Identifiers
What OpenQuestion holds
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.