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Annu Rev Immunol. 2008;26:481-511. doi: 10.1146/annurev.immunol.26.021607.090236.

The biochemistry of somatic hypermutation.

Author information

1
Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA. jpeled@aecom.yu.edu

Abstract

Affinity maturation of the humoral response is mediated by somatic hypermutation of the immunoglobulin (Ig) genes and selection of higher-affinity B cell clones. Activation-induced cytidine deaminase (AID) is the first of a complex series of proteins that introduce these point mutations into variable regions of the Ig genes. AID deaminates deoxycytidine residues in single-stranded DNA to deoxyuridines, which are then processed by DNA replication, base excision repair (BER), or mismatch repair (MMR). In germinal center B cells, MMR, BER, and other factors are diverted from their normal roles in preserving genomic integrity to increase diversity within the Ig locus. Both AID and these components of an emerging error-prone mutasome are regulated on many levels by complex mechanisms that are only beginning to be elucidated.

[Indexed for MEDLINE]

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