To establish active infection, inhaled Mycobacterium tuberculosis (Mtb) must overcome the physical barriers of the upper respiratory tract and invade alveolar macrophages. Clearance of the pathogen from the lower airways requires a fine-tuned interaction of immune cells, most prominently T-lymphocytes and macrophages. There is definite evidence for the critical role of CD4+ T-lymphocytes in activating the antimicrobial activity of macrophages (1). The evidence for a contribution of CD8+ T cells in protection against Mtb is steadily increasing through conclusive animal studies and strong circumstantial evidence from human ex vivo and in vitro experiments (2–7). CD8+ T-lymphocytes promote the control of Mtb infection indirectly by the release of macrophage-activating cytokines or directly by the injection of cytotoxic molecules into infected macrophages (8). The granular molecules perforin, granzyme B, and granulysin interact to define an antimicrobial effector pathway leading to direct