期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 105, 期 45, 页码 17463-17468出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0808043105
关键词
apoptosis; necrosis; NF kappa B; Ripk1 autophagy
资金
- National Institutes of Health [AI037988]
- National Institute of Diabetes and Digestive and Kidney Disease Training [T32DK007233]
T cells enigmatically require caspase-8, an inducer of apoptosis, for antigen-driven expansion and effective antiviral responses, and yet the pathways responsible for this effect have been elusive. A defect in caspase-8 expression does not affect progression through the cell cycle but causes an abnormally high rate of cell death that is distinct from apoptosis and does not involve a loss of NF kappa B activation. Instead, antigen or mitogen activated Casp8-deficient T cells exhibit an alternative type of cell death similar to programmed necrosis that depends on receptor interacting protein (Ripk1). The selective genetic ablation of caspase-8, NF kappa B, and Ripk1, reveals two forms of cell death that can regulate virus-specific T cell expansion.
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