Regulation of Oxidative Stress Responses by Ataxia-Telangiectasia Mutated Is Required for T Cell Proliferation
| Autor: | John Iacomini, Jessamyn Bagley, Gyanesh Singh |
|---|---|
| Rok vydání: | 2007 |
| Předmět: |
CD3 Complex
T-Lymphocytes T cell Immunology Receptors Antigen T-Cell Apoptosis Cell Cycle Proteins Ataxia Telangiectasia Mutated Proteins Protein Serine-Threonine Kinases Biology Lymphocyte Activation medicine.disease_cause Mice Interleukin 21 CD28 Antigens medicine Animals Immunology and Allergy Cytotoxic T cell Immunodeficiency chemistry.chemical_classification Mice Inbred BALB C Reactive oxygen species Tumor Suppressor Proteins T-cell receptor medicine.disease Cell biology DNA-Binding Proteins Mice Inbred C57BL Oxidative Stress medicine.anatomical_structure chemistry Reactive Oxygen Species Oxidative stress |
| Zdroj: | The Journal of Immunology. 178:4757-4763 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.178.8.4757 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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