Koonin Eugene V, Zhang Feng
National Center for Biotechnology Information, National Library of Medicine, Bethesda, MD, USA.
Broad Institute of MIT and Harvard, Cambridge, MA, USA.
Bioessays. 2017 Jan;39(1):1-9. doi: 10.1002/bies.201600186. Epub 2016 Nov 29.
Host-pathogen arms race is a universal, central aspect of the evolution of life. Most organisms evolved several distinct yet interacting strategies of anti-pathogen defense including resistance to parasite invasion, innate and adaptive immunity, and programmed cell death (PCD). The PCD is the means of last resort, a suicidal response to infection that is activated when resistance and immunity fail. An infected cell faces a decision between active defense and altruistic suicide or dormancy induction, depending on whether immunity is "deemed" capable of preventing parasite reproduction and consequent infection of other cells. In bacteria and archaea, immunity genes typically colocalize with PCD modules, such as toxins-antitoxins, suggestive of immunity-PCD coupling, likely mediated by shared proteins that sense damage and "predict" the outcome of infections. In type VI CRISPR-Cas systems, the same enzyme that inactivates the target RNA might execute cell suicide, in a case of ultimate integration of immunity and PCD.
宿主-病原体军备竞赛是生命进化的一个普遍且核心的方面。大多数生物体进化出了几种不同但相互作用的抗病原体防御策略，包括对寄生虫入侵的抗性、先天免疫和适应性免疫，以及程序性细胞死亡（PCD）。程序性细胞死亡是最后的手段，是在抗性和免疫失效时被激活的对感染的自杀性反应。一个被感染的细胞面临着在主动防御与利他性自杀或诱导休眠之间做出抉择，这取决于免疫是否“被认为”有能力阻止寄生虫繁殖以及随之而来的对其他细胞的感染。在细菌和古细菌中，免疫基因通常与程序性细胞死亡模块共定位，例如毒素-抗毒素，这暗示着免疫与程序性细胞死亡的耦合，可能是由感知损伤并“预测”感染结果的共享蛋白介导的。在VI型CRISPR-Cas系统中，使靶RNA失活的同一种酶可能会执行细胞自杀，这是免疫与程序性细胞死亡最终整合的一个例子。
