Abstract
Activation-induced cytidine deaminase (AID) is expressed in germinal center B cells and initiates the events that lead to somatic hypermutation and class switch recombination of immunoglobulin genes. In addition to this fundamental role in immune diversification, aberrant targeting of AID activity contributes to point mutations and translocations of oncogenes associated with B-cell lymphoma. This review discusses recent findings on the role of AID in lymphomagenesis. AID is expressed in many malignancies of mature B-cell origin and contributes to the development of lymphoma in several mouse models. The mechanism that guides AID to its genetic target is unknown and may be relatively nonspecific, as numerous nonimmunoglobulin genes appear to be targeted by AID in both normal and neoplastic B cells. Indeed, AID binds to genes on every chromosome throughout the genome and can induce double-stranded DNA breaks that lead to chromosome translocations at these sites. Emerging evidence supports a key role of AID in lymphomagenesis through genome-wide off-target induction of point mutations and chromosome translocations. Additional work is needed to further define the full scope and consequences of off-target AID activity in human lymphoma as well as to understand the protective mechanisms that break down during the development and progression of disease.
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