Our finding thatpolyclonal CD4+ effector T cell responses diminish in chronicinfection suggests that this may be a general phenomenon in tuberculosis.Importantly though, the higher frequency of P25TCRTh1 cell activation observed inCPE85B-infected mice diminished at a later time point as it did in H37Rv infection,implying that other mechanisms, especially impairment of MHC II antigen presentationby M. tuberculosis, exist to limit effector T cell activationduring chronic infection in vivo. Here, CD4 is linked to infection.