Activation-induced Cytidine Deaminase in B Cell Immunity and Cancers.
- Author:
Seok Rae PARK
1
Author Information
- Publication Type:Review
- Keywords: Activation-induced cytidine deaminase; B cell; Antibody; Cancer
- MeSH: B-Lymphocytes; Burkitt Lymphoma; Cell Transformation, Neoplastic; Cytidine; Cytidine Deaminase; DNA; Genetic Processes; Germinal Center; Hand; Immunity, Humoral; Immunoglobulins; Leukemia, B-Cell; Lymphoma; Point Mutation; Protein Processing, Post-Translational; Recombination, Genetic; RNA, Messenger; T-Lymphocytes; Transcriptional Activation
- From:Immune Network 2012;12(6):230-239
- CountryRepublic of Korea
- Language:English
- Abstract: Activation-induced cytidine deaminase (AID) is an enzyme that is predominantly expressed in germinal center B cells and plays a pivotal role in immunoglobulin class switch recombination and somatic hypermutation for antibody (Ab) maturation. These two genetic processes endow Abs with protective functions against a multitude of antigens (pathogens) during humoral immune responses. In B cells, AID expression is regulated at the level of either transcriptional activation on AID gene loci or post-transcriptional suppression of AID mRNA. Furthermore, AID stabilization and targeting are determined by post-translational modifications and interactions with other cellular/nuclear factors. On the other hand, aberrant expression of AID causes B cell leukemias and lymphomas, including Burkitt's lymphoma caused by c-myc/IgH translocation. AID is also ectopically expressed in T cells and non-immune cells, and triggers point mutations in relevant DNA loci, resulting in tumorigenesis. Here, I review the recent literatures on the function of AID, regulation of AID expression, stability and targeting in B cells, and AID-related tumor formation.
