抑制泰勒氏病毒诱导的受感染小鼠巨噬细胞凋亡会导致坏死性凋亡。
Inhibition of Theiler's virus-induced apoptosis in infected murine macrophages results in necroptosis.
作者信息
Son Kyung-No, Lipton Howard L
机构信息
Department of Microbiology-Immunology, University of Illinois at Chicago, Chicago, IL, United States.
Department of Microbiology-Immunology, University of Illinois at Chicago, Chicago, IL, United States.
出版信息
Virus Res. 2015 Jan 2;195:177-82. doi: 10.1016/j.virusres.2014.10.017. Epub 2014 Oct 27.
Abstract
In mice Theiler's murine encephalomyelitis virus (TMEV) persists in macrophages that eventually undergo apoptosis. TMEV infection of macrophages in culture induces apoptosis through the intrinsic pathway, restricting virus yields. We show that inhibition of TMEV-induced apoptosis leads to phosphorylation of receptor interacting protein 1 (RIP1), localization of RIP1 and RIP3 to mitochondria, ROS production independent of MAPK activation and programmed necrosis (necroptosis). Blocking both apoptosis and necroptosis restored virus yields.
摘要
在小鼠中，泰勒氏鼠脑脊髓炎病毒（TMEV）在巨噬细胞中持续存在，这些巨噬细胞最终会发生凋亡。培养的巨噬细胞感染TMEV会通过内源性途径诱导凋亡，从而限制病毒产量。我们发现，抑制TMEV诱导的凋亡会导致受体相互作用蛋白1（RIP1）磷酸化，RIP1和RIP3定位于线粒体，产生不依赖于丝裂原活化蛋白激酶（MAPK）激活的活性氧（ROS）并引发程序性坏死（坏死性凋亡）。同时阻断凋亡和坏死性凋亡可恢复病毒产量。
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