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Adv Immunol. 2011;110:1-26. doi: 10.1016/B978-0-12-387663-8.00005-3.

AID targeting in antibody diversity.

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Laboratory of Molecular Immunology, The Rockefeller University, New York, USA.


Antibody maturation requires class switch recombination (CSR) and somatic hypermutation (SHM), both of which are initiated by activation-induced cytidine deaminase (AID). AID deaminates cytosine residues resulting in mismatches that are differentially processed to produce double-strand breaks in Ig switch (S) regions that lead to CSR, or to point mutations in variable (V) exons resulting in SHM. Although AID was first thought to be Ig-specific, recent work indicates that it also targets a diverse group of non-Ig loci, including genes such as Bcl6 and c-myc, whose modification by AID results in lymphoma-associated mutations and translocations. Here, we review the recent literature on AID targeting and the role for transcriptional stalling in recruitment of this enzyme to Ig and non-Ig loci. We propose a model for AID recruitment based on transcriptional stalling, which reconciles several of the key features of SHM, CSR, and lymphoma-associated translocation.

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