Immunoglobulin (Ig) class switch recombination (CSR) is the process occurring in mature B cells that diversifies the effector component of antibody responses. CSR is initiated by the activity of the B cell-specific enzyme activation-induced cytidine deaminase (AID), which leads to the formation of programmed DNA double-strand breaks (DSBs) at the Ig heavy chain (Igh) locus. Mature B cells use a multilayered and complex regulatory framework to ensure that AID-induced DNA breaks are channeled into productive repair reactions leading to CSR, and to avoid aberrant repair events causing lymphomagenic chromosomal translocations. Here, we review the DNA repair pathways acting on AID-induced DSBs and their functional interplay, with a particular focus on the latest developments in their molecular composition and mechanistic regulation.

免疫球蛋白 (Ig) 类转换重组 (CSR) 是发生在成熟 B 细胞中的过程，它使抗体反应的效应子成分多样化。CSR 由 B 细胞特异性酶激活诱导胞苷脱氨酶 (AID) 的活性启动，导致 Ig 重链 ( Igh ) 处程序性 DNA 双链断裂 (DSB) 的形成) 轨迹。成熟的 B 细胞使用多层复杂的调控框架来确保 AID 诱导的 DNA 断裂被引导到导致 CSR 的生产性修复反应中，并避免导致淋巴瘤染色体易位的异常修复事件。在这里，我们回顾了作用于 AID 诱导的 DSB 的 DNA 修复途径及其功能相互作用，特别关注其分子组成和机械调节的最新发展。