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Curr Opin Immunol. 2001 Oct;13(5):543-8.

Human genetic defects in class-switch recombination (hyper-IgM syndromes).

Author information

1
Institut National de la Santé et de la Recherche Médicale (INSERM) U429, Hôpital Necker-Enfants Malades, 149 Rue de Sèvres, Cedex 15, Paris, France. durandy@necker.fr

Abstract

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-kappaB activation and the essential role of a newly described molecule, activation-induced cytidine deaminase (AID), in B cell terminal differentiation.

PMID:
11544001
[Indexed for MEDLINE]

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