期刊
SEMINARS IN IMMUNOLOGY
卷 24, 期 4, 页码 293-300出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.smim.2012.05.005
关键词
Mismatch repair; Class switch recombination; Somatic hypermutation; Activation-induced deaminase; Double-strand breaks; Cytosine deamination; Epigenetic; Antibody diversity
类别
资金
- NIH [CA72649, CA102705, CA76329, CA93484]
- National Women's Division of the Albert Einstein College of Medicine
- Spanish Ministerio de Economia y Competitividad [PTQ-11-04774]
The creation of a highly diverse antibody repertoire requires the synergistic activity of a DNA mutator, known as activation-induced deaminase (AID), coupled with an error-prone repair process that recognizes the DNA mismatch catalyzed by AID. Instead of facilitating the canonical error-free response, which generally occurs throughout the genome, DNA mismatch repair (MMR) participates in an error-prone repair mode that promotes A:T mutagenesis and double-strand breaks at the immunoglobulin (Ig) genes. As such, MMR is capable of compounding the mutation frequency of AID activity as well as broadening the spectrum of base mutations; thereby increasing the efficiency of antibody maturation. We here review the current understanding of this MMR-mediated process and describe how the MMR signaling cascade downstream of AID diverges in a locus dependent manner and even within the Ig locus itself to differentially promote somatic hypermutation (SHM) and class switch recombination (CSR) in B cells. (C) 2012 Elsevier Ltd. All rights reserved.
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