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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Curr Opin Microbiol. 2015 Nov 27;29:56–62. doi: 10.1016/j.mib.2015.11.001

Figure 1. Yersinia vs. host immunity.

Figure 1

(a) Evasion of host signaling pathways by the type III secretion system. YpkA association with actin monomers targets actin-regulating proteins to inhibit phagocytosis. In neutrophils, delivery of YopH leads to dephosphorylation of SLP-76, PRAM-1 and SKAP-HOM, down-regulating calcium signaling and production of anti-inflammatory IL-10, while extrusion of microbicidal neutrophil DNA (NETosis) is inhibited in a T3SS-dependent manner. In macrophages, specific YopM isoforms utilize an internal motif (YLTD) within the protein to directly sequester caspase-1 while other YopM isoforms target caspase-1 via the host scaffolding protein IQGAP1. (b) Triggering of host responses by the type III secretion system. Toll-like receptor 4 detection of the needle protein YscF activates NF-κB, inducing expression and production of pro-inflammatory cytokines. In contrast, inhibition of NF-κB and MAP kinase pathways by YopJ drives RIP kinase- and caspase-8-dependent activation of inflammatory caspase-1. Activation of caspase-1 also occurs upon translocation of YopB and YopD into the host cell cytosol. Additionally, sensing of YopE GTPase-activating protein activity can trigger killing of phagosomal Yersinia.