Irf8-deficient mice, then, display defective Th1 responses (absence of antigen specific and IFNγ producing CD4+ T cells) [22], enhanced Th17 responses [23], and are susceptible to in vivo infection with many intracellular pathogens [18], [24]–[26] including tuberculosis [22] and blood-stage malaria [27]. This evidence concerns the gene IFNG and infection.