| Abstract: |
Class switch recombination (CSR) represents one of the hallmark DNA transactions that activated B cells execute during the generation of a humoral immune response to diversify the production of their antibody isotypes. Initiated by the B cell-specific DNA mutator activation-induced cytidine deaminase, CSR requires the coordinated interplay of an assortment of factors and processes including transcription, RNA metabolism, DNA and protein modifications, generation and sensing of programmed double-stranded breaks, canonical and non-canonical DNA repair and remodelling of the immunoglobulin gene locus architecture. Here, we review the molecular events required for CSR, the mechanisms involved in regulating these events and the consequences of aberrant CSR on the genomic stability of B cells. We also briefly discuss the evolution of CSR in relation to the emergence of cytidine deaminase and DNA switch regions and the co-opting of DNA repair factors. © 2024 Elsevier Ltd. All rights are reserved, including those for text and data mining, AI training, and similar technologies. Published by Elsevier Ltd. All rights reserved. |
