caused by Mycobacterium tuberculosis is a potentially serious infectious
disease that affects millions of people globally. It is one of the top ten
causes of death worldwide and remains a major health problem infecting 10
million people every year. Mycobacterium tuberculosis is a gram negative, slow
growing acid-fast bacterium that is primarily transmitted by the respiratory
route. It remains in the latent phase in about one third of the world
population of which only 10% of the people develop active TB disease later in
life. The strength of the host immune system determines whether the bacteria
will remain in latency or develop the disease in an infected individual. M.tb
after entering the alveolar passages first contacts the resident macrophages.
In addition, dendritic cells are known to play a very important role in the
early stages of infection since they have better antigen presentation
properties than macrophages and apparently play a key role in activating T
lymphocytes with specific M.tb antigens. Since dendritic cells are migratory,
unlike differentiated macrophages they are also efficient in producing better
host effector responses against the infection. The pathogen largely remains undetected within the host by modulating cell survival of various cell types for
its own advantages by altering
pathways that are responsible for recognition and elimination of the pathogen.
We have previously shown that M.tb on its own as well as in
conjunction with HIV inhibits macrophage apoptosis. In this study we wished to
decipher the role of apoptosis during M.tb infection in dendritic cells which
are the key players in driving T cell mediated responses. To that end we infected
Dendritic cells with M.tb antigen Rv 3416 earlier reported by our lab.
Rv 3416 or whiB transcription regulatory factor (whiB) is a day 5
antigen expressed by M.tb infected macrophages 24 hours post infection and is known to suppress host responses to
M.tb in both Dendritic cells and macrophages.