Activation-Induced cytidine Deaminase (AID) initiates affinity maturation and isotype switching by deaminating deoxycytidines within immunoglobulin genes, leading to somatic hypermutation (SHM) and class switch recombination (CSR). AID thus potentiates the humoral response to clear pathogens. Marking the 20th anniversary of the discovery of AID, we review the current understanding of AID function. We discuss AID biochemistry and how error-free forms of DNA repair are co-opted to prioritize mutagenesis over accuracy during antibody diversification. We discuss the regulation of DNA double-strand break (DSB) repair pathways during CSR. We describe genomic targeting of AID as a multilayered process involving chromatin architecture, cis- and trans-acting factors, and determining mutagenesis – distinct from AID occupancy at loci that are spared from mutation.

激活诱导的胞苷脱氨酶（AID）通过使免疫球蛋白基因内的脱氧胞苷脱氨基，启动亲和力成熟和同种型转换，从而导致体细胞超突变（SHM）和类别转换重组（CSR）。因此，AID增强了对清除病原体的体液反应。纪念AID发现20周年，我们回顾了对AID功能的最新了解。我们讨论了AID生物化学以及如何选择无错误形式的DNA修复来在抗体多样化期间优先考虑诱变而不是准确性。我们讨论了在企业社会责任过程中DNA双链断裂（DSB）修复途径的调控。我们将AID的基因组靶向描述为涉及染色质结构，顺式和反式的多层过程作用因子，并确定诱变–与避免突变的基因座上的AID占用率不同。