This is associated with the pro-inflammatory effects of type I IFN: recruitment of innate immune cells to the site of infection (mainly pDC and monocytes); increases in pro-inflammatory cytokines and chemokines in BALF (IL-6, IP-10, MCP-1, MIP-1α); and increases in the frequency of respiratory epithelial cell apoptosis. This evidence concerns the gene CXCL10 and infection.