Figure 5.

Synergism of Caspase-1/11 and RipK3 signaling promotes control of ST infection. WT, RipK3^−/minus;, Caspase-1,11^−/minus; and Caspase-1,11^−/minus;RipK3^−/minus; mice were infected with ST-OVA (10³, i.v.). On day 7, bacterial burden was evaluated in the spleens of infected mice (a). Survival of infected mice was monitored for up to 60 days (b). The numbers of OVA_257-264 (SIINFEKL)-specific CD8⁺ T cells were evaluated in the spleens of infected mice by staining with anti-CD8 antibody and H2-K^b-SIINFEKL tetramers (c). Naive spleen cells (control- CFLE^low and OVA_257-264-pulsed- CFSE^hi) were injected into mice that were infected with ST-OVA 6 days prior. At 24 h post spleen cell transfer, the fate of transferred cells was evaluated in the spleens of infected mice (d,e). Mice were infected as described above, and CD8⁺ T cells were purified on day 7 post-infection, and the expression of IFN−γ evaluated by ELISPOT assay with/without OVA_257-264 pulsed naive spleen cells (f,g). Data is shown as mean ±SEM and is representative of 2–3 separate experiments