Abstract:
:The immune system is capable of recognizing and eliminating an enormous array of pathogens due to the extremely diverse antigen receptor repertoire of T and B lymphocytes. However, the development of lymphocytes bearing receptors with unique specificities requires the generation of programmed double strand breaks (DSBs) coupled with bursts of proliferation, rendering lymphocytes susceptible to mutations contributing to oncogenic transformation. Consequently, mechanisms responsible for monitoring global genomic integrity must be activated during lymphocyte development to limit the oncogenic potential of antigen receptor locus recombination. Mutations in ATM (ataxia-telangiectasia mutated), a kinase that coordinates DSB monitoring and the response to DNA damage, result in impaired T-cell development and predispose to T-cell leukemia. Here, we review recent evidence providing insight into the mechanisms by which ATM promotes normal lymphocyte development and protects from neoplastic transformation.
journal_name
Immunol Revjournal_title
Immunological reviewsauthors
Matei IR,Guidos CJ,Danska JSdoi
10.1111/j.0105-2896.2006.00361.xkeywords:
subject
Has Abstractpub_date
2006-02-01 00:00:00pages
142-58eissn
0105-2896issn
1600-065Xpii
IMR361journal_volume
209pub_type
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