Production of the neutrophil attractant CXCL1 in infected cells was inhibited by type I IFN signaling as indicated by the increased secretion from type I IFN receptor-deficient macrophages (Supplementary Fig. 2c) and, accordingly, it demonstrated an essentially reciprocal pattern of secretion as compared to IFNβ upon infection with our mutants (Fig. 1f). This evidence concerns the gene IFNB1 and infection.