The continuing HIV/
AIDS epidemic and the spread of multi-
drug resistant Mycobacterium tuberculosis has led to the perpetuation of the worldwide
tuberculosis epidemic. While M. bovis BCG is widely used as a
vaccine, it lacks efficacy in preventing
pulmonary tuberculosis in adults [1]. To combat this ongoing scourge,
vaccine development for
tuberculosis is a global priority. Most infected individuals develop long-lived protective immunity, which controls and contains M.
tuberculosis in a T cell-dependent manner. An effective T cells response determines whether the
infection resolves or develops into clinically evident disease. Consequently, there is great interest in determining which T cells subsets mediate anti-mycobacterial immunity, delineating their effector functions, and evaluating whether vaccination can elicit these T cells subsets and induce protective immunity. CD4(+) T cells are critical for resistance to M.
tuberculosis in both humans and rodent models. CD4(+) T cells are required to control the initial
infection as well as to prevent recrudescence in both humans and mice [2]. While it is generally accepted that class II MHC-restricted CD4(+) T cells are essential for immunity to
tuberculosis, M.
tuberculosis infection elicits CD8(+) T cells responses in both people and in experimental animals. CD8(+) T cells are also recruited to the lung during M.
tuberculosis infection and are found in the
granulomas of infected people. Thus, how CD8(+) T cells contribute to overall immunity to
tuberculosis and whether
antigens recognized by CD8(+) T cells would enhance the efficacy of
vaccine strategies continue to be important questions.