Mice lacking the STING signaling pathway generate a protective adaptive immune response following <i>L. monocytogenes</i> reinfection.

<p>B6, <i>Gt</i>, <i>IRF3^−/−</i> and <i>IRF3/7^−/−</i> mice were immunized intravenously with 10³ CFU ActA⁻Lm-OVA (Δ<i>actA</i>) (open circles) or administered PBS (closed circles) and 30–38 days later challenged with 2×10⁵ CFU WT Lm-OVA. Three days post challenge, <b>A</b>. bacterial CFU in the spleens and livers were enumerated. The dashed line represents the limit of detection. <b>B</b>. Splenocytes were stained with anti-mouse CD8, CD44 and K^b/OVA_257–264 tetramer and analyzed by flow cytometry. Quantitative analysis shows the total number of K^b/OVA_257–264 tetramer⁺ CD44⁺ CD8⁺ T cells/spleen. <b>C</b>. Splenocytes were either unstimulated (un) or stimulated with OVA_257–264 (OVA) or LLO_190–201 (LLO) peptides followed by intracellular staining with anti-mouse IFN-γ, TNF-α and IL-2. Quantitative analysis shows the percentage of IFN-γ⁺/TNF-α⁺/IL-2⁻ (solid bars) or IFN-γ⁺/TNF-α⁺/IL-2⁺ (lined bars) within the CD8⁺ or CD4⁺ population. Data are presented as the cumulative results from 5–12 (<b>A</b>), 3–6 (<b>B</b>) or 2–4 (<b>C</b>, mean ± SEM) independent experiments using at least five mice per group. Asterisks represent significance as compared to Δ<i>actA</i>-immunized B6 mice (*p<0.05, **p<0.005, ***p<0.0005).