Durandy A
Inserm U429, Hôpital Necker-Enfants Malades, 149 Rue de Sèvres, Paris, France.
Biochem Soc Trans. 2002 Aug;30(4):815-8. doi: 10.1042/bst0300815.
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 kappa B 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.
最近在人类中发现了几种与类别转换重组相关的基因缺陷，这些缺陷会导致高IgM综合征。除了众所周知的CD40配体与CD40相互作用的作用外，这些病症明确证明了CD40介导的核因子κB激活的必要性，以及一种最近描述的分子——激活诱导的胞苷脱氨酶在有效的体液免疫反应（包括类别转换重组和高亲和力抗体的产生）中的重要作用。
