Immunoglobulin class switch recombination: study through human natural mutants
Immunoglobulin class switch recombination: study through human natural mutants
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DOI：
10.1098/rstb.2008.0210
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发表时间：
2009-03-12
影响因子：
6.3
通讯作者：
Durandy, Anne
中科院分区：
文献类型：
--
作者：
Durandy, Anne
人类免疫球蛋白类开关重组缺陷是分析类开关重组机制的良好模型。除了CD40L/CD40相互作用缺陷外，其他缺陷是由于固有的b细胞缺陷造成的。最近对其中一些分子基础的阐明使得描述抗体成熟过程中涉及的分子事件成为可能。激活诱导的（胞苷）脱氨酶（AID）和尿嘧啶- n-糖基化酶缺陷已经证明了AID作为开关区和可变区DNA损伤的诱导剂的作用。然而，大多数CSR缺陷在分子上仍未定义。它们的特征将有助于更好地理解企业社会责任中涉及的复杂机制。
Immunoglobulin class switch recombination deficiencies in humans are exquisite models to analyse the mechanisms of class switch recombination (CSR). Besides defects in CD40L/CD40 interaction, others result from an intrinsic B-cell deficiency. The recent elucidation of the molecular basis of some of them has made it possible to delineate the molecular events involved in antibody maturation. Activation-induced (cytidine) deaminase (AID) and uracil-N-glycosylase deficiencies have demonstrated the role of AID as the inducer of DNA lesions in switch and variable regions. However, most of these CSR deficiencies remain molecularly undefined. Their characterization would lead to a better understanding of the complex machinery involved in CSR.