At 16 dpi during the infection, it became clear that the absence of IL-23 leads to a more Th2 response since it presented the higher levels of IL-4, IL-5, and IL-33 in the lungs, and a marked reduction of the capacity to produce Th17 profile cytokines such as IL-17A and IL-22, and proinflammatory cytokines such as IL-1β and TNF-α (Figure S2). The gene discussed is IL22; the disease is infection.