To catch a thief: regulated RIPK1 post-translational modifications as a fail-safe system to detect and overcome...

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.