Affinity maturation of the humoral response is mediated by somatic hypermutation of the immunoglobulin (Ig) genes and selection of higher-affinity B cell clones. Activation-induced cytidine deaminase (AID) is the first of a complex series of proteins that introduce these point mutations into variable regions of the Ig genes. AID deaminates deoxycytidine residues in single-stranded DNA to deoxyuridines, which are then processed by DNA replication, base excision repair (BER), or mismatch repair (MMR). In germinal center B cells, MMR, BER, and other factors are diverted from their normal roles in preserving genomic integrity to increase diversity within the Ig locus. Both AID and these components of an emerging error-prone mutasome are regulated on many levels by complex mechanisms that are only beginning to be elucidated.

中文翻译：

---

体细胞超突变的生物化学。

体液反应的亲和力成熟是由免疫球蛋白（Ig）基因的体细胞超突变和更高亲和力的B细胞克隆的选择介导的。激活诱导的胞苷脱氨酶（AID）是一系列复杂的蛋白质中的第一个，这些蛋白质将这些点突变引入Ig基因的可变区。AID将单链DNA中的脱氧胞苷残基脱氨为脱氧尿苷，然后通过DNA复制，碱基切除修复（BER）或错配修复（MMR）对其进行处理。在生发中心B细胞中，MMR，BER和其他因素偏离了它们在维持基因组完整性方面的正常作用，从而增加了Ig基因座内的多样性。AID和新出现的容易出​​错的突变体的这些组件都在许多层面上受到复杂机制的调节，这些机制才刚刚被阐明。