ArticlePloS one2008
Activation-induced cytidine deaminase deficiency causes organ-specific autoimmune disease.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 64 citations in OpenAlex.
- Microbial influences on severity and sex bias of systemic autoimmunity.Immunological reviews · 2024Review
- Activation-induced cytidine deaminase expression by thymic B cells promotes T-cell tolerance and limits autoimmunity.iScience · 2023Article
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
- Polymorphic Immune Mechanisms Regulate Commensal Repertoire.Cell reports · 2019Article
- A Drosophila genetic screen for suppressors of S6kinase-dependent growth identifies the F-box subunit Archipelago/FBXW7.Molecular genetics and genomics : MGG · 2019Article
- Activation-induced cytidine deaminase deficiency accelerates autoimmune diabetes in NOD mice.JCI insight · 2018Article
- Aberrant expression of interleukin-10 and activation-induced cytidine deaminase in B cells from patients with Behçet's disease.Biomedical reports · 2017Article
- Selective IgM Deficiency: Clinical and Laboratory Features of 17 Patients and a Review of the Literature.Journal of clinical immunology · 2017Review
- 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
- Functions and Malfunctions of Mammalian DNA-Cytosine Deaminases.Chemical reviews · 2016Review
- Self-Antigen-Driven Thymic B Cell Class Switching Promotes T Cell Central Tolerance.Cell reports · 2016Article
- Primary antibody deficiencies.Nature reviews. Immunology · 2013Review
- Microbiota and autoimmunity.Cold Spring Harbor perspectives in biology · 2013Review
- Potential roles of activation-induced cytidine deaminase in promotion or prevention of autoimmunity in humans.Autoimmunity · 2013Review
- Quorum sensing contributes to activated IgM-secreting B cell homeostasis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Revisiting the old link between infection and autoimmune disease with commensals and T helper 17 cells.Immunologic research · 2012Review
- LINE-1 retroelements complexed and inhibited by activation induced cytidine deaminase.PloS one · 2012Article
- Pathogenesis of autoimmunity in common variable immunodeficiency.Frontiers in immunology · 2012Article
- Activation-induced cytidine deaminase (AID) is required for B-cell tolerance in humans.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Activation-induced cytidine deaminase mediates central tolerance in B cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation-induced cytidine deaminase (AID) expressed by germinal center B cells is a central regulator of somatic hypermutation (SHM) and class switch recombination (CSR). Humans with AID mutations develop not only the autosomal recessive form of hyper-IgM syndrome (HIGM2) associated with B cell hyperplasia, but also autoimmune disorders by unknown mechanisms. We report here that AID-/- mice spontaneously develop tertiary lymphoid organs (TLOs) in non-lymphoid tissues including the stomach at around 6 months of age. At a later stage, AID-/- mice develop a severe gastritis characterized by loss of gastric glands and epithelial hyperplasia. The disease development was not attenuated even under germ-free (GF) conditions. Gastric autoantigen -specific serum IgM was elevated in AID-/- mice, and the serum levels correlated with the gastritis pathological score. Adoptive transfer experiments suggest that autoimmune CD4+ T cells mediate gastritis development as terminal effector cells. These results suggest that abnormal B-cell expansion due to AID deficiency can drive B-cell autoimmunity, and in turn promote TLO formation, which ultimately leads to the propagation of organ-specific autoimmune effector CD4+ T cells. Thus, AID plays an important role in the containment of autoimmune diseases by negative regulation of autoreactive B cells.
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