Activation-Induced Cytidine Deaminase in Antibody Diversification and Chromosome Translocation

摘要: DNA damage, rearrangement, and mutation of the human genome are basis carcinogenesis thought to be avoided at all costs. An exception is adaptive immune system where lymphocytes utilize programmed damage effect antigen receptor diversification. Both B T diversify their receptors through RAG1/2 mediated recombination, but cells undergo two additional processes--somatic hypermutation (SHM) class-switch recombination (CSR), both initiated by activation-induced cytidine deaminase (AID). AID deaminates cytidines in resulting U:G mismatches that processed into point mutations SHM or double-strand breaks CSR. Although activity focused Immunoglobulin (Ig) gene loci, it also targets a wide array non-Ig genes including oncogenes associated with lymphomas. Here, we review molecular regulation, targeting, initiation CSR SHM, as well AID's role generating chromosome translocations contribute lymphomagenesis.