Review
Nature Reviews Immunology 2, 605-614 (August 2002) | doi:10.1038/nri858
AID and mismatch repair in antibody diversification
Alberto Martin1 & Matthew D. Scharff1 About the authors
Abstract
In response to antigen, B cells undergo a series of specialized genetic events to produce the 'ideal' population of antibodies to prevent and eradicate infections. Although these events — somatic hypermutation, gene conversion and class-switch recombination — have been recognized for many years, the enzymes that are involved have remained elusive. The recent discovery that activation-induced cytidine deaminase (AID) and the mismatch repair (MMR) system are involved in these processes has led to new models of the biochemical events that generate antibody diversity. However, there is still considerable uncertainty about the mechanism of action of AID, and there are differing viewpoints about the role of MMR.
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Author affiliations
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Department of Cell Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Chanin 403, Bronx, New York 10461, USA.
Email: amartin@aecom.yu.edu; Email: scharff@aecom.yu.edu
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region but rarely in S
regions prior to class switch recombination
