AID and somatic hypermutation

Robert W. Maul, Patricia J. Gearhart

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

In response to an assault by foreign organisms, peripheral B cells can change their antibody affinity and isotype by somatically mutating their genomic DNA. The ability of a cell to modify its DNA is exceptional in light of the potential consequences of genetic alterations to cause human disease and cancer. Thus, as expected, this mechanism of antibody diversity is tightly regulated and coordinated through one protein, activation-induced deaminase (AID). AID produces diversity by converting cytosine to uracil within the immunoglobulin loci. The deoxyuracil residue is mutagenic when paired with deoxyguanosine, since it mimics thymidine during DNA replication. Additionally, B cells can manipulate the DNA repair pathways so that deoxyuracils are not faithfully repaired. Therefore, an intricate balance exists which is regulated at multiple stages to promote mutation of immunoglobulin genes, while retaining integrity of the rest of the genome. Here we discuss and summarize the current understanding of how AID functions to cause somatic hypermutation.

Original languageEnglish (US)
Title of host publicationAdvances in Immunology
PublisherAcademic Press Inc.
Pages159-191
Number of pages33
EditionC
DOIs
StatePublished - 2010

Publication series

NameAdvances in Immunology
NumberC
Volume105
ISSN (Print)0065-2776
ISSN (Electronic)1557-8445

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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