FIG. 9.

Model for the pathogenic role of YopM in plague. Both macrophages and NK cells are hypothesized to be important targets of infection by Y. pestis. Delivery of YopM into macrophages promotes a decrease in the expression of IL-12, IL-18, and IL-15. YopM delivery into NK cells inhibits expression of IL-15Rα, which promotes systemic depletion of NK cells. The depletion of NK cells limits the early production of IFN-γ during infection, which affects innate immunity by decreasing the capacity of macrophages to become activated early during infection. A reduced ability to generate an effective Th1 adaptive immune response occurs due to reduced expression of IL-12 and IL-18. The result is unchecked growth of yersiniae during both the innate and adaptive phases of the immune response.