Mycobacterium tuberculosis (Mtb) has been evolving with its human host for many generations and has developed the capacity to manipulate the human immune response. One working model of the interaction between Mtb and the human host is that the bacterium induces both a strong inflammatory and a strong acquired immune response and then actively regulates these responses. The induction and subsequent regulation then results in an infectious lesion in the lung while maintaining a relatively ambulatory host. CD4 T cells play a critical yet contradictory role in this process by both controlling disseminated disease while promoting the development of the lesion in the lung that mediates transmission. It is not surprising that our ability to vaccinate against tuberculosis (TB) has not been totally successful as we are essentially mimicking what the bacterium does in vivo. In order to overcome the current impasse in vaccine development we need to define the phenotype of CD4 T cells which mediate protection and to determine those bacterial and host factors which regulate the effective function of these cells at the site of infection. I will discuss the phenotype of the T cell and the type of inflammation which can regulate the function of the T cell in the lung.