Trigg Ben J, Ferguson Brian J
Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.
Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB2 1QP, UK.
Curr Opin Virol. 2015 Dec;15:56-62. doi: 10.1016/j.coviro.2015.08.001. Epub 2015 Aug 27.
DNA is potently immunostimulatory, and self-DNA is packaged in the nucleus or mitochondria allowing it to remain silent to cell-intrinsic sensors. However, damaged or mislocalised self-DNA is sensed by our innate immune systems, resulting in the production of type I interferons (IFNI), chemokines and inflammatory cytokines. During DNA virus infection the detection of viral DNA genomes by pattern recognition receptors (PRRs) is essential for the initiation of IFNI responses and host defence against these pathogens. It is intriguing that a number of molecular mechanisms have been found to be common to both of these DNA-induced stress responses and this has potentially important consequences for both sides of the host/pathogen arms race.
DNA具有强大的免疫刺激作用，自身DNA被包裹在细胞核或线粒体中，使其对细胞内固有传感器保持沉默。然而，受损或定位错误的自身DNA会被我们的先天免疫系统感知，从而导致I型干扰素（IFNⅠ）、趋化因子和炎性细胞因子的产生。在DNA病毒感染期间，模式识别受体（PRR）对病毒DNA基因组的检测对于启动IFNⅠ反应和宿主抵御这些病原体至关重要。有趣的是，已发现许多分子机制在这两种DNA诱导的应激反应中是共同的，这对宿主/病原体军备竞赛的双方都可能产生重要影响。
