| First Author | Bagley J | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 8 | Pages | 4757-63 |
| PubMed ID | 17404255 | Mgi Jnum | J:145205 |
| Mgi Id | MGI:3833816 | Doi | 10.4049/jimmunol.178.8.4757 |
| Citation | Bagley J, et al. (2007) Regulation of oxidative stress responses by ataxia-telangiectasia mutated is required for T cell proliferation. J Immunol 178(8):4757-63 |
| abstractText | Mutations in the gene encoding ataxia-telangiectasia (A-T) mutated (Atm) cause the disease A-T, characterized by immunodeficiency, the molecular basis of which is not known. Following stimulation through the TCR, Atm-deficient T cells and normal T cells in which Atm is inhibited undergo apoptosis rather than proliferation. Apoptosis is prevented by scavenging reactive oxygen species (ROS) during activation. Atm therefore plays a critical role in T cell proliferation by regulating responses to ROS generated following T cell activation. The inability of Atm-deficient T cells to control responses to ROS is therefore the molecular basis of immunodeficiency associated with A-T. |
