程序性细胞死亡
细胞生物学
细胞凋亡
坏死性下垂
裂谷1
生物
抗原
坏死
T细胞
半胱氨酸蛋白酶
肿瘤坏死因子α
细胞
免疫系统
免疫学
生物化学
遗传学
作者
Irene L. Ch’en,Daniel R. Beisner,Alexei Degterev,C. Lynch,Junying Yuan,Alexander Hoffmann,Stephen Μ. Hedrick
标识
DOI:10.1073/pnas.0808043105
摘要
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 NFκB 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, NFκB, and Ripk1, reveals two forms of cell death that can regulate virus-specific T cell expansion.
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