Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Department of Microbiology, Immunology, and Molecular Genetics, University of Texas Health San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Cell Host Microbe. 2017 Apr 12;21(4):415-416. doi: 10.1016/j.chom.2017.03.014.
RIPK3 and RIPK1 limit virus spread by executing either apoptotic or necroptotic cell death in response to infection. In a recent issue of Cell, Daniels et al. (2017) unveil an unexpected cell death-independent requirement of RIP kinase activity in coordinating neuroinflammation, restricting West Nile virus pathogenesis in neurons.
RIPK3 和 RIPK1 通过响应感染执行凋亡或坏死细胞死亡来限制病毒传播。在最近一期的《细胞》杂志上，Daniels 等人（2017）揭示了 RIP 激酶活性在协调神经炎症中的一个出乎意料的与细胞死亡无关的要求，从而限制了西尼罗河病毒在神经元中的发病机制。
