In the absence of IFN-γ, which is required to control IL-17-producing T cells [25], enhanced expression of IL-17 could contribute to either protective mechanisms resulting in the inhibition of mycobacterial growth rate as observed in our experiments at the later stage of infection, or to the severe lung pathology typical for GKO mice infected with pathogenic mycobacteria, or to both of these effects. The gene discussed is IL17A; the disease is infection.