Immunity through DNA deamination

Michael S. Neuberger, Reuben S. Harris, Javier Di Noia, Svend K. Petersen-Mahrt

Research output: Contribution to journalReview articlepeer-review

197 Scopus citations

Abstract

Functional antibody genes assembled by V(D)J joining are subsequently diversified by somatic hypermutation, gene conversion and class-switch recombination. Recent evidence indicates that all three processes are caused by the deamination of cytosine to uracil at sites within the immunoglobulin (Ig) loci, with the pattern of diversification depending on the pathway used for resolving the initiating dU-dG lesion. Whereas DNA deamination targeted to the endogenous Ig locus triggers a program of somatic gene diversification that underpins adaptive immunity, deamination targeted to foreign DNA might have arisen initially as a form of innate immunity. Furthermore, the observation that members of the DNA deaminase family can target inappropriate genes suggests they might also contribute to mutations during genome evolution, as well as in cancer.

Original languageEnglish (US)
Pages (from-to)305-312
Number of pages8
JournalTrends in Biochemical Sciences
Volume28
Issue number6
DOIs
StatePublished - Jun 1 2003

Bibliographical note

Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.

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