Consistent with this model, wefound that a recombinant strain of M. tuberculosis engineered tomaintain the expression of fbpB at high levels during chronicinfection (CPE85B) was attenuated during the chronic phase of infection in astrictly CD4+ T cell dependent manner, indicating thatdown-regulation of fbpB and limitation of antigen availability isimportant for evasion of adaptive immunity by M. tuberculosis.Treatment of infected mice with synthetic Ag85B peptide 25 also increasedCD4+ effector T cell IFN-γ responses and significantlyreduced the bacterial burden in the lungs. Here, IFNG is linked to infection.