Hyper-IgM syndromes: a model for studying the regulation of class switch recombination and somatic hypermutation generation
Hyper-IgM syndromes: a model for studying the regulation of class switch recombination and somatic hypermutation generation
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DOI：
10.1042/bst0300815
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发表时间：
2002-08-01
影响因子：
3.9
通讯作者：
Durandy, A
中科院分区：
文献类型：
--
作者：
Durandy, A
最近在人类中描述了几种导致高IgM综合征的类开关重组的遗传缺陷。除了CD40-配体-CD40相互作用的众所周知的作用外，这些病理明确地证明了CD40介导的核因子kappaB激活的必要性，以及最近描述的一个分子的重要作用，激活诱导的胞苷脱氨酶在有效的体液反应中包括类别切换重组和高亲和力抗体的产生。
Several genetic defects in class switch recombination, which lead to a hyper-IgM syndrome, have been described recently in humans. In addition to the well known role of CD40-ligand-CD40 interaction, these pathologies demonstrate definitively the requirement of CD40-mediated nuclear factor kappaB activation and the essential role of a recently described molecule, the activation-induced cytidine deaminase in an efficient humoral response, which includes class switch recombination and the production of high-affinity antibodies.