The fact that Th1 cells play a central role in protection against Tb is based on several factors: (i) mice lacking CD4+ T cells, IFN-γ and IL-12 signaling or T-bet are highly susceptible to infection (4); (ii) individuals with genetic deficiencies in IFN-γ and IL-12 signaling are unable to control mycobacterial infections (52); (iii) HIV patients co-infected with Tb have increased risk of developing active disease (53). Here, CD4 is linked to infection.