Since type I IFN contributes to pathogenesis of intracellular bacterial infection [14–16] and type I IFN-inducible genes were highly represented in both the blood and tissue transcriptional signature during L. monocytogenes infection we sought to determine how a lack of type I IFN receptor signaling in Ifnar1-/- mice affected the global transcriptional response to infection as compared to that observed in the WT controls (C57BL/6 background). This evidence concerns the gene IFNAR1 and bacterial infectious disease.