Lee Seung-Hwan, Miyagi Takuya, Biron Christine A
Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.
Trends Immunol. 2007 Jun;28(6):252-9. doi: 10.1016/j.it.2007.04.001. Epub 2007 Apr 27.
Natural killer (NK) cells use multiple mechanisms to defend against viral infections, and different stimuli can activate these antiviral effects. When engaged, receptors for innate cytokines produced during infections and for ligands on target cells can both induce NK cell cytotoxicity and the production of cytokines. These stimuli use different classes of intracellular signaling pathways to elicit the overlapping responses. What is the advantage of using different roads to the same ends? One answer might be in the nature of the alternative regulatory pathways that are in place to control the respective stimuli. A model of flexibility in accessing NK cell function, in the context of negative regulation of particular intracellular signaling pathways, is proposed here.
自然杀伤（NK）细胞利用多种机制抵御病毒感染，不同的刺激可激活这些抗病毒效应。当被激活时，感染期间产生的先天性细胞因子受体以及靶细胞上的配体受体均可诱导NK细胞的细胞毒性和细胞因子的产生。这些刺激利用不同类别的细胞内信号通路引发重叠反应。殊途同归的优势何在？一种答案可能在于为控制各自刺激而存在的替代调节途径的性质。本文提出了一种在特定细胞内信号通路负调控背景下获取NK细胞功能的灵活性模型。
