Although we cannot rule out that potential microbiota differences between WT and pearl mice contribute to the enhanced susceptibility of AP-3-/- mice to infection, pearl mice with a comparable STm burden at day 3 of infection had impaired IL-1β and IL-18 responses in MLN–one of the first sites of STm entry, where pro-inflammatory cytokine production is required to prevent bacterial dissemination–suggesting an intrinsic defect in inflammasome activation and consistent with our in vitro results in bone marrow-derived and splenic DCs. Here, IL1B is linked to infection.