Mycobacterium tuberculosis infects about one-third of the world’s population, causing≈ 3 million deaths annually (Dye et al., 1999). The organism is a slow-growing bacillus that is transmitted by the respiratory route. Although it is capable of causing disease in most organs, pulmonary involvement is most common. Soon after infection, the bacilli are phagocytosed by alveolar macrophages and survive within early phagosomes. Innate immune responses directed by macrophages predominate early in infection. Subsequent recruitment of dendritic cells leads to cell-mediated responses involving CD4+ and CD8+ T cells and eventual granuloma formation (for a review, see Fenton and Vermeulen, 1996; Flynn and Chan, 2001). The vast majority of immunocompetent individuals are able to contain, but not eliminate, the pathogen in pulmonary granulomas, leading to latent tuberculosis infection (Manabe and Bishai, 2000). In a small minority of cases, through unclear mechanisms, persistent bacilli can reactivate to form disease many years to decades after initial infection.

An interesting feature of mycobacteria is the extraordinarily high lipid content of the cell envelope, constituting up to 40% of their dry weight (Anderson, 1940). In addition to conferring unique tinctorial properties, which aid in the diagnosis of infected clinical specimens, the mycobacterial cell envelope (see Fig. 1) is important in directing host–pathogen interactions (Besra and Chatterjee, 1994; Brennan and Nikaido, 1995).