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The role of activation-induced deaminase in antibody diversification and genomic instability

  • Immunology in Colorado
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An Erratum to this article was published on 27 July 2013

Abstract

More than a decade ago, activation-induced deaminase (AID) was identified as the initiator for somatic hypermutation (SHM) and class switch recombination (CSR). Since then, tremendous progress has been achieved toward elucidating how AID functions. AID targets the highly repetitive switch regions of the immunoglobulin heavy chain (IgH) locus to induce DNA double-strand breaks (DSBs), which can be rejoined, leading to switch of constant regions of antibody. When targeting to variable region exons of IgH and IgL loci, AID predominantly induces point mutations, termed SHM, resulting in increased affinity of antibody for antigen. While SHM and CSR enhance antibody diversity, AID-initiated DSBs and mutations may predispose B cells to carcinogenesis. This review focuses on the mechanisms that provide the specificity of AID targeting to Ig loci and the role of AID in genomic instability.

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Acknowledgments

I thank Drs. Zhangguo Chen, Shan Zha, and Ming Tian for comments. I apologize to those whose work was not cited due to length restrictions. This work was supported by a University of Colorado School of Medicine start-up fund, Leukemia Research Foundation, and Boettcher Foundation (to J.H.W.) J.H.W. is a recipient of Boettcher Foundation Webb-Waring Biomedical Research Award. The author declares no conflict of interest.

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    Jing H. Wang

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Wang, J.H. The role of activation-induced deaminase in antibody diversification and genomic instability. Immunol Res 55, 287–297 (2013). https://doi.org/10.1007/s12026-012-8369-4

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