The creation of a highly diverse antibody repertoire requires the synergistic activity of a DNA mutator, known as activation-induced deaminase (AID), coupled with an error-prone repair process that recognizes the DNA mismatch catalyzed by AID. Instead of facilitating the canonical error-free response, which generally occurs throughout the genome, DNA mismatch repair (MMR) participates in an error-prone repair mode that promotes A:T mutagenesis and double-strand breaks at the immunoglobulin (Ig) genes. As such, MMR is capable of compounding the mutation frequency of AID activity as well as broadening the spectrum of base mutations; thereby increasing the efficiency of antibody maturation. We here review the current understanding of this MMR-mediated process and describe how the MMR signaling cascade downstream of AID diverges in a locus dependent manner and even within the Ig locus itself to differentially promote somatic hypermutation (SHM) and class switch recombination (CSR) in B cells.

高度多样化的抗体库的创建需要 DNA 增变因子（称为激活诱导脱氨酶 (AID)）的协同活性，以及​​识别由 AID 催化的 DNA 错配的容易出错的修复过程。DNA 错配修复 (MMR) 不是促进通常发生在整个基因组中的典型无错误反应，而是参与一种容易出错的修复模式，促进 A:T 突变和免疫球蛋白 (Ig) 基因的双链断裂。因此，MMR 能够复合 AID 活性的突变频率以及拓宽碱基突变的谱；从而提高抗体成熟的效率。