Another Function for AID

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Science  23 Jun 2006:
Vol. 312, Issue 5781, pp. 1719
DOI: 10.1126/science.312.5781.1719a

Activation-induced cytidine deaminase (AID) plays a pivotal role in the immune system, controlling antibody class switching and generating diversity through somatic hypermutation of immunoglobulin genes. AID is also part of a larger group of deaminases, which include the antiretroviral APOBEC family members.

Gourzi et al. explored the possibility that AID might possess a similar capacity for protection against retroviruses and found that cells from mice lacking AID were indeed less able to cope with a replication-deficient form of the transforming Abelson murine leukemia virus (Ab-MLV). In response to infection, AID activity was induced in the bone marrow, extending its territory beyond the B cell germinal center. Furthermore, mice succumbed to transformed B cell tumors more rapidly if they lacked AID, and showed a corresponding failure to control cellular proliferation. AID activity induced phosphorylation of the cell cycle checkpoint kinase Chk1 and increased the sensitivity of host cells to killing by natural killer (NK) cells by up-regulating NK cell receptor ligands. These observations fit well with a model in which generalized DNA damage caused by widespread AID-induced mutations in transcribed genes prompts both checkpoint arrest and elimination by the immune system. It will now be interesting to see how broadly the scope for AID in protecting host from pathogen might extend. — SJS

Immunity 24, 10.1016/j.immuni.2006.03.021 (2006).

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