Any pathogen worth its salt has mechanisms to evade, subvert, or antagonize host innate immune responses induced by pattern recognition receptors. Resistance against such pathogens therefore requires alternative means to activate protective immune responses. Intriguingly, the receptors that regulate antimicrobial gene expression are coupled to cell death pathways that are activated by blockade of NF-κB and MAPK signaling. In this review, we discuss the regulation of apoptosis in response to pathogen disruption of immune signaling and the role of this cell death response in protection against such pathogens. Stanley often observed that bacterial pathogens are excellent cell biologists and immunologists, and he noted that studying pathogen-host interactions could pave the way to new insights about host biology. Indeed, how Yersinia and other pathogens disrupt innate immune signaling has provided new insight into these pathways and revealed new ways to think about immunogenic properties of apoptosis during bacterial infection.

中文翻译：

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抓小偷：调节的RIPK1翻译后修饰是一种故障安全系统，可以检测和克服病原体对免疫信号的破坏。

任何有价值的病原体都有逃避，破坏或拮抗模式识别受体诱导的宿主固有免疫反应的机制。因此，对此类病原体的抗药性需要其他手段来激活保护性免疫反应。有趣的是，调节抗微生物基因表达的受体与细胞死亡途径偶联，该途径通过阻断NF-κB和MAPK信号传导而激活。在这篇综述中，我们讨论了响应于免疫信号的病原体破坏而对凋亡的调节，以及这种细胞死亡反应在针对此类病原体的保护中的作用。斯坦利经常观察到细菌病原体是出色的细胞生物学家和免疫学家，并且他指出研究病原体与宿主之间的相互作用可以为对宿主生物学的新见解铺平道路。确实，