Collectively, our transcriptome and histology data show that type I IFN and IFN-γ signaling are both involved in control of neutrophilic inflammation during T. gondii infection, likely contributing to the increased pathology seen in the Ifnar−/−, Ifngr−/−, and double Ifnar−/− × Ifngr−/− as compared to Wild type mice upon infection, over-and-above any type I IFN and IFN-γ induced pathways of microbial control. The gene discussed is IFNGR1; the disease is infection.