Activation induced cytidine deaminase (AID) plays a central role in the vertebrate adaptive immune response, initiating immunoglobulin (Ig) somatic hypermutation (SHM) and class-switch recombination (CSR). AID converts deoxycytosine (dC) in the DNA to deoxyuridine (dU), causing a DNA base-pairing mismatch. How this mismatch is recognised and resolved determines whether the site will undergo mutation, recombination or high-fidelity repair. Although AID action is essential for antibody diversification it is also known to act upon many non-Ig genes where it can cause tumourigenic mutations and translocations. Although much is known about the pathways of Ig diversification, there is still very little known about the mechanisms that target AID to its sites of action and regulate the different repair processes that can participate at these sites.

中文翻译：

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调节活化诱导的胞苷脱氨酶的靶向和活性的机制。

激活诱导的胞苷脱氨酶 (AID) 在脊椎动物适应性免疫反应中发挥核心作用，启动免疫球蛋白 (Ig) 体细胞超突变 (SHM) 和类别转换重组 (CSR)。AID 将 DNA 中的脱氧胞嘧啶 (dC) 转化为脱氧尿苷 (dU)，从而导致 DNA 碱基配对错配。如何识别和解决这种错配决定了该位点是否会发生突变、重组或高保真修复。尽管 AID 作用对于抗体多样化是必不可少的，但也已知它作用于许多非 Ig 基因，在这些基因上它可能导致致瘤性突变和易位。尽管人们对 Ig 多样化的途径了解很多，但对于将 AID 靶向其作用位点并调节可参与这些位点的不同修复过程的机制仍然知之甚少。