Human genetic defects in class-switch recombination (hyper-IgM syndromes)
A Durandy, T Honjo - Current opinion in immunology, 2001 - Elsevier
A Durandy, T Honjo
Current opinion in immunology, 2001•ElsevierSeveral genetic defects in class-switch recombination, leading to hyper-IgM syndromes,
have been recently described in humans. Besides the well-known role of interaction
between CD40-ligand and CD40, these pathological conditions definitively demonstrate the
requirement of CD40-mediated NF-κB activation and the essential role of a newly described
molecule, activation-induced cytidine deaminase (AID), in B cell terminal differentiation.
have been recently described in humans. Besides the well-known role of interaction
between CD40-ligand and CD40, these pathological conditions definitively demonstrate the
requirement of CD40-mediated NF-κB activation and the essential role of a newly described
molecule, activation-induced cytidine deaminase (AID), in B cell terminal differentiation.
Several genetic defects in class-switch recombination, leading to hyper-IgM syndromes, have been recently described in humans. Besides the well-known role of interaction between CD40-ligand and CD40, these pathological conditions definitively demonstrate the requirement of CD40-mediated NF-κB activation and the essential role of a newly described molecule, activation-induced cytidine deaminase (AID), in B cell terminal differentiation.
Elsevier
