Although IFN-γ is upregulated during infection and particularly expressed by these transdifferentiated Th1 cells, this cytokine alone seems not to be the key factor of bacterial clearance, since neither INFg-/- mice have higher bacterial burden after infection nor does anti-IFN-γ treatment reverse the phenotype in conditional T-bet-deficiency in Th17 cells. This evidence concerns the gene TBX21 and infection.