Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways.
Viral infection and the evolution of caspase 8-regulated apoptotic and necrotic death pathways.
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DOI：
10.1038/nri3131
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发表时间：
2011-12-23
期刊：
影响因子：
--
通讯作者：
Kaiser WJ
中科院分区：
文献类型：
--
作者：
Mocarski ES;Upton JW;Kaiser WJ
病原体特异性地针对依赖于caspase 8的凋亡细胞死亡途径和依赖于受体相互作用蛋白1(RIPK1；也称为RIPK1)和RIPK3(也称为RIPK3)的坏死细胞死亡途径。当缺乏Fas相关死亡结构域蛋白(FADD)或caspase 8的小鼠的中期死亡被RIP1或RIP3消除逆转时，这两条细胞死亡途径的基本共同调节出现了，这表明一种比先前认识的更紧密的关系。因此，哺乳动物在胚胎发生期间需要caspase 8活性来抑制RIP1和RIP3激酶，这是两个不同的细胞死亡过程之间对话的一部分，这两个过程共同发挥加强宿主对疱疹病毒等细胞内病原体的防御作用。
Pathogens specifically target both the caspase 8-dependent apoptotic cell death pathway and the necrotic cell death pathway that is dependent on receptor-interacting protein 1 (RIP1; also known as RIPK1) and RIP3 (also known as RIPK3). The fundamental co-regulation of these two cell death pathways emerged when the midgestational death of mice deficient in FAS-associated death domain protein (FADD) or caspase 8 was reversed by elimination of RIP1 or RIP3, indicating a far more entwined relationship than previously appreciated. Thus, mammals require caspase 8 activity during embryogenesis to suppress the kinases RIP1 and RIP3 as part of the dialogue between two distinct cell death processes that together fulfil reinforcing roles in the host defence against intracellular pathogens such as herpesviruses.