C-type lectins in immunity to Mycobacterium tuberculosis.

Tuberculosis (TB) remains one of the leading causes of death due to a single infectious agent, Mycobacterium tuberculosis, with nearly 2 million deaths per year (1). Most individuals exposed to the bacillus develop a nonpathological form, latent TB, with only a small minority (5 to 10%) developing active disease. It is estimated that one third of the human population worldwide may have latent M. tuberculosis infection. Latent TB is characterized by an efficient immune response that contains the infection in a nonpathological and noncontagious state, within a specific, dynamic structure called the granuloma. Interactions between M. tuberculosis and the immune system play a crucial role in determining the outcome of the disease, and are mediated by various pattern recognition receptors (PRRs) expressed in cells of the innate immune system and in nonimmune cells. These interactions may modulate the immune response in favor of the bacillus, by allowing it to persist within host phagocytes. They may also favor the host, by inducing immune defenses, such as autophagy, phagosome maturation, apoptosis and various bactericidal mechanisms.