An increase in certain neutrophil-associated genes from the IL-17 pathway/granulocytes module (L11), was observed in all IFN-receptor-deficient mice upon infection (Cluster i and ii, Fig. 8a, b), although ll17a itself was not detectable in T. gondii infected tissues, except in the absence of IFN-γ signaling (Supplementary Data 14). Here, IL17A is linked to infection.