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Induction and Assessment of Class Switch Recombination in Purified Murine B Cells
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Published on: August 13, 2010

Immunoglobulin class switch recombination: study through human natural mutants

Anne Durandy1

  • 1INSERM, U768, Paris 75015, France. anne.durandy@inserm.fr

Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
|November 15, 2008
PubMed

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.

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