Innate immune sensors can recognize when host cells are irrevocably compromised by pathogens, and in response can trigger programmed cell death (pyroptosis, apoptosis, and necroptosis). Innate sensors can directly bind microbial ligands; for example, NAIP/NLRC4 detects flagellin/rod/needle, whereas caspase-11 detects lipopolysaccharide. Other sensors are guards that monitor normal function of cellular proteins; for instance, pyrin monitors Rho GTPases, whereas caspase-8 and receptor-interacting protein kinase (RIPK)3 guards RIPK1 transcriptional signaling. Some proteins that need to be guarded can be duplicated as decoy domains, as seen in the integrated decoy domains within NLRP1 that watch for microbial attack. Here, we discuss the evolutionary battle between pathogens and host innate immune sensors/guards, illustrated by the Red Queen hypothesis. We discuss in depth four pathogens, and how they either fail in this evolutionary race (Chromobacterium violaceum, Burkholderia thailandensis), or how the evolutionary race generates increasingly complex virulence factors and host innate immune signaling pathways (Yersinia species, and enteropathogenic Escherichia coli [EPEC]).

中文翻译：

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与细菌毒力因子的进化竞赛中的程序性细胞死亡。

先天免疫传感器可以识别宿主细胞何时被病原体不可逆转地破坏，并作为响应触发程序性细胞死亡（细胞焦亡、细胞凋亡和坏死性凋亡）。先天传感器可以直接结合微生物配体；例如，NAIP/NLRC4 检测鞭毛蛋白/杆/针，而 caspase-11 检测脂多糖。其他传感器是监测细胞蛋白质正常功能的卫士。例如，pyrin 监测 Rho GTPases，而 caspase-8 和受体相互作用蛋白激酶 (RIPK)3 保护 RIPK1 转录信号。一些需要保护的蛋白质可以被复制为诱饵域，如 NLRP1 中用于监视微生物攻击的集成诱饵域中所见。在这里，我们讨论病原体和宿主先天免疫传感器/守卫之间的进化战，红皇后假说说明了这一点。我们深入讨论了四种病原体，以及它们如何在这个进化种族（紫色色杆菌、泰国伯克霍尔德氏菌）中失败，或者进化种族如何产生越来越复杂的毒力因子和宿主先天免疫信号通路（耶尔森菌属和肠道致病性大肠杆菌[EPEC] ]）。