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. 2005 Sep 19;202(6):761–769. doi: 10.1084/jem.20050193

Figure 1.

Figure 1.

Animals with targeted gene deletion in the IL-12, IL-17, and IL-23 signaling pathways demonstrate increased mortality during intrapulmonary K. pneumoniae infection. (A) WT C57BL/6, IL-23 p19−/−, IL-12 p35−/−, IL-12 p40−/−, or IL-17R−/− mice were challenged with 104 CFU intratracheal K. pneumoniae and survival was recorded every 12 h (n = 16–20 per group). IL-12 p40 knockout mice showed the greatest susceptibility to infection (*P < 0.01 compared with C57BL/6 [log rank test]). Survival differences between IL-23 p19−/−, IL-17R−/−, and IL-12 p35−/− mice were not statistically significant. (B) WT and p19−/− mice were also challenged with a lower dose (103 CFU) of bacteria, demonstrating significant mortality in p19−/− mice to a sublethal dose of K. pnuemoniae (*P < 0.01 compared with WT mice; n = 10 per group).