title: Mutations, kataegis and translocations in B cells: understanding AID promiscuous activity.
abstract: As B cells engage in the immune response, they express activation-induced cytidine deaminase (AID) to initiate the hypermutation and recombination of immunoglobulin genes, which are crucial processes for the efficient recognition and disposal of pathogens. However, AID must be tightly controlled in B cells to minimize off-target mutations, which can drive chromosomal translocations and the development of B cell malignancies, such as lymphomas. Recent genomic and biochemical analyses have begun to unravel the mechanisms of how AID-mediated deamination is targeted outside immunoglobulin genes. Here, we discuss the transcriptional and topological features that are emerging as key drivers of AID promiscuous activity.
authors.affiliation: Genomics and Immunity, National Institute of Arthritis and Musculoskeletal and Skin Diseases-National Cancer Institute (NIAMS-NCI), National Institutes of Health, Bethesda, Maryland 20892, USA.
authors.forename: Rafael
authors.initials: R
authors.lastname: Casellas
authors.affiliation: Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA.
authors.forename: Uttiya
authors.initials: U
authors.lastname: Basu
authors.affiliation: Immunology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.|Immunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences, New York, New York 10065, USA.
authors.forename: William T
authors.initials: WT
authors.lastname: Yewdell
authors.affiliation: Immunology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.
authors.forename: Jayanta
authors.initials: J
authors.lastname: Chaudhuri
authors.affiliation: Laboratory of Molecular Immunology, The Rockefeller University, New York, New York 10065, USA.
authors.forename: Davide F
authors.initials: DF
authors.lastname: Robbiani
authors.affiliation: Institut de Recherches Cliniques de Montréal, H2W 1R7 Montréal, Québec, Canada.|Department of Medicine, Université de Montréal, H3C 3J7 Montréal, Québec, Canada.
authors.forename: Javier M
authors.initials: JM
authors.lastname: Di Noia
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D003564:Cytidine Deaminase / Q000276:immunology*; D006801:Humans; D017578:Immunoglobulin Class Switching / Q000276:immunology*; D016393:Lymphoma, B-Cell / Q000235:genetics* / Q000276:immunology*; D009154:Mutation; D027041:Somatic Hypermutation, Immunoglobulin / Q000276:immunology; D014178:Translocation, Genetic; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
chemical_list: D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase