The immunoglobulin (Ig) repertoire achieves functional diversification through several somatic alterations of the Ig locus. One of these processes, somatic hypermutation (SHM), deposits point mutations into the variable region of the Ig gene to generate higher-affinity variants. Activation-induced cytidine deaminase (AID) converts cytidine to uridine to initiate the hypermutation process. Error-prone versions of DNA repair are believed to then process these lesions into a diverse spectrum of point mutations. We review the current understanding of the molecular mechanisms and regulation of SHM, and also discuss emerging ideas which merit further exploration.

中文翻译：

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免疫球蛋白体细胞超突变。

免疫球蛋白（Ig）库通过Ig基因座的几种体细胞改变实现功能多样化。这些过程之一是体细胞超突变（SHM），将点突变沉积到Ig基因的可变区中以生成更高亲和力的变异体。激活诱导的胞苷脱氨酶（AID）将胞苷转化为尿苷以启动超突变过程。据信，DNA修复容易出错，然后将这些病灶加工成各种各样的点突变。我们回顾了目前对SHM分子机制和调控的理解，并讨论了值得进一步探索的新兴思想。