ArticleEuropean journal of immunology2014
Production of IgG autoantibody requires expression of activation-induced deaminase in early-developing B cells in a mouse model of SLE.
Article in European journal of immunology, 2014. 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.
- The mechanisms of human lymphoid chromosomal translocations and their medical relevance.Critical reviews in biochemistry and molecular biology · 2022Article
- Diversity upon diversity: linking DNA double-strand break repair to blood cancer health disparities.Trends in cancer · 2022Review
- Mechanistic basis for chromosomal translocations at the E2A gene and its broader relevance to human B cell malignancies.Cell reports · 2021Article
- Small Molecule Inhibitors of Activation-Induced Deaminase Decrease Class Switch Recombination in B Cells.ACS pharmacology & translational science · 2021Article
- Autoimmune B Cell Repertoire in a Mouse Model of Sjögren's Syndrome.Frontiers in immunology · 2021Article
- Base Excision Repair in the Immune System: Small DNA Lesions With Big Consequences.Frontiers in immunology · 2020Review
- The Plasticity of Newly Formed B Cells.Journal of immunology (Baltimore, Md. : 1950) · 2019Review
- Anti-double Stranded DNA Antibodies: Origin, Pathogenicity, and Targeted Therapies.Frontiers in immunology · 2019Review
- Regulatory effects of four ginsenoside monomers in humoral immunity of systemic lupus erythematosus.Experimental and therapeutic medicine · 2018Article
- Interleukin-33 Contributes Toward Loss of Tolerance by Promoting B-Cell-Activating Factor of the Tumor-Necrosis-Factor Family (BAFF)-Dependent Autoantibody Production.Frontiers in immunology · 2018Article
- Anti‑IL‑39 (IL‑23p19/Ebi3) polyclonal antibodies ameliorate autoimmune symptoms in lupus‑like mice.Molecular medicine reports · 2018Article
- BCR and Endosomal TLR Signals Synergize to Increase AID Expression and Establish Central B Cell Tolerance.Cell reports · 2017Article
- Accelerated Systemic Autoimmunity in the Absence of Somatic Hypermutation in 564Igi: A Mouse Model of Systemic Lupus with Knocked-In Heavy and Light Chain Genes.Frontiers in immunology · 2017Article
- Mechanisms of human lymphoid chromosomal translocations.Nature reviews. Cancer · 2016Review
- Cooperation of ETV6/RUNX1 and BCL2 enhances immunoglobulin production and accelerates glomerulonephritis in transgenic mice.Oncotarget · 2016Article
- Activation-Induced Cytidine Deaminase Expression in Human B Cell Precursors Is Essential for Central B Cell Tolerance.Immunity · 2015Article
- Female Bias in Systemic Lupus Erythematosus is Associated with the Differential Expression of X-Linked Toll-Like Receptor 8.Frontiers in immunology · 2015Article
- IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
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7 authors at 2 institutions in 2 countries.
Funding
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of pathogenic IgG antinuclear antibodies. Pathogenic IgG autoantibody production requires B-cell activation, leading to the production of activation-induced deaminase (AID) and class switching of IgM genes to IgG. To understand how and when B cells are activated to produce these IgG autoantibodies, we studied cells from 564Igi, a mouse model of SLE. 564Igi mice develop a disease profile closely resembling that found in human SLE patients, including the presence of IgG antinucleic acid Abs. We have generated 564Igi mice that conditionally express an activation-induced cytidine deaminase transgene (Aicda(tg) ), either in all B cells or only in mature B cells. Here, we show that class-switched pathogenic IgG autoantibodies were produced only in 564Igi mice in which AID was functional in early-developing B cells, resulting in loss of tolerance. Furthermore, we show that the absence of AID in early-developing B cells also results in increased production of self-reactive IgM, indicating that AID, through somatic hypermutation, contributes to tolerance. Our results suggest that the pathophysiology of clinical SLE might also be dependent on AID expression in early-developing B cells.
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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.