ArticleProceedings of the National Academy of Sciences of the United States of America2011
Activation-induced cytidine deaminase mediates central tolerance in B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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Who cites it
74 citing papers in PubMed, 105 citations in OpenAlex.
- Distributed clonal deletion prevents autoimmune disease progression.Cell reports · 2026Article
- AID and TET2 cooperate to demethylate Irf4 for plasma cell fate in germinal center B cells.The Journal of experimental medicine · 2026Article
- Distributed Clonal Deletion Prevents Autoimmune Disease Progression.bioRxiv : the preprint server for biology · 2026Article
- Age-associated immune dysregulation and B cell dysfunction drive severe outcomes in SFTSV infection.PLoS pathogens · 2025Article
- Integration of spatial and single-cell data across modalities with weakly linked features.Nature biotechnology · 2024Article
- Antigen-presenting autoreactive B cells activate regulatory T cells and suppress autoimmune arthritis in mice.The Journal of experimental medicine · 2023Article
- Review
- LAPTM5 mediates immature B cell apoptosis and B cell tolerance by regulating the WWP2-PTEN-AKT pathway.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The mechanisms of human lymphoid chromosomal translocations and their medical relevance.Critical reviews in biochemistry and molecular biology · 2022Article
- Recall of B cell memory depends on relative locations of prime and boost immunization.Science immunology · 2022Article
- Diversity upon diversity: linking DNA double-strand break repair to blood cancer health disparities.Trends in cancer · 2022Review
- Positive and negative selection shape the human naive B cell repertoire.The Journal of clinical investigation · 2022Article
- Activation induced cytidine deaminase: An old friend with new faces.Frontiers in immunology · 2022Review
- Article
- Continuous Culture of Mouse Primary B Lymphocytes by Forced Expression ofJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Mechanistic basis for chromosomal translocations at the E2A gene and its broader relevance to human B cell malignancies.Cell reports · 2021Article
- Activation-induced deaminase is critical for the establishment of DNA methylation patterns prior to the germinal center reaction.Nucleic acids research · 2021Article
- Do Transgenerational Epigenetic Inheritance and Immune System Development Share Common Epigenetic Processes?Journal of developmental biology · 2021Review
- Active DNA demethylation-The epigenetic gatekeeper of development, immunity, and cancer.Advanced genetics (Hoboken, N.J.) · 2021Review
- The uracil-DNA glycosylase UNG protects the fitness of normal and cancer B cells expressing AID.NAR cancer · 2020Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The Aicda gene product, activation-induced cytidine deaminase (AID), initiates somatic hypermutation, class-switch recombination, and gene conversion of Ig genes by the deamination of deoxycytidine, followed by error-prone mismatch- or base-excision DNA repair. These processes are crucial for the generation of genetically diverse, high affinity antibody and robust humoral immunity, but exact significant genetic damage and promote cell death. In mice, physiologically significant AID expression was thought to be restricted to antigen-activated, mature B cells in germinal centers. We now demonstrate that low levels of AID in bone marrow immature and transitional B cells suppress the development of autoreactivity. Aicda(-/-) mice exhibit significantly increased serum autoantibody and reduced capacity to purge autoreactive immature and transitional B cells. In vitro, AID deficient immature/transitional B cells are significantly more resistant to anti-IgM-induced apoptosis than their normal counterparts. Thus, early AID expression plays a fundamental and unanticipated role in purging self-reactive immature and transitional B cells during their maturation in the bone marrow.
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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.