期刊
NATURE REVIEWS IMMUNOLOGY
卷 16, 期 3, 页码 164-176出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nri.2016.2
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- NCI NIH HHS [T32 CA009149, P30 CA008748] Funding Source: Medline
- NIAID NIH HHS [R21 AI112602] Funding Source: Medline
As B cells engage in the immune response, they express activation-induced cytidine deaminase (AID) to initiate the hypermutation and recombination of immunoglobulin genes, which are crucial processes for the efficient recognition and disposal of pathogens. However, AID must be tightly controlled in B cells to minimize off-target mutations, which can drive chromosomal translocations and the development of B cell malignancies, such as lymphomas. Recent genomic and biochemical analyses have begun to unravel the mechanisms of how AID-mediated deamination is targeted outside immunoglobulin genes. Here, we discuss the transcriptional and topological features that are emerging as key drivers of AID promiscuous activity.
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