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1564045 
Journal Article 
Immunology of tuberculosis 
Raja, A 
2012 
Indian Journal of Medical Research
ISSN: 0971-5916 
136 
213-232 
Tuberculosis is a major health problem throughout the world
causing large number of deaths, more than that from any other single infectious disease. The
review attempts to summarize the information available on host immune response to Mycobacterium
tuberculosis. Since the main route of entry of the causative agent is the respiratory route,
alveolar macrophages are the important cell types, which combat the pathogen. Various aspects of
macrophage-mycobacterium interactions and the role of macrophage in host response such as binding
of M. tuberculosis to macrophages via surface receptors, phagosome-lysosome fusion, mycobacterial
growth inhibition/killing through free radical based mechanisms such as reactive oxygen and
nitrogen intermediates; cytokine-mediated mechanisms; recruitment of accessory immune cells for
local inflammatory response and presentation of antigens to T cells for development of acquired
immunity have been described. The role of macrophage apoptosis in containing the growth of the
bacilli is also discussed. The role of other components of innate immune response such as natural
resistance associated macrophage protein (Nramp), neutrophils, and natural killer cells has been
discussed. The specific acquired immune response through CD4 T cells, mainly responsible for
protective Th1 cytokines and through CD8 cells bringing about cytotoxicity, also has been
described. The role of CD-I restricted CD8(+) T cells and non-MHC restricted gamma/delta T cells
has been described although it is incompletely understood at the present time. Humoral immune
response is seen though not implicated in protection. The value of cytokine therapy has also been
reviewed. Influence of the host human leucocyte antigens (HLA) on the susceptibility to disease
is discussed. Mycobacteria are endowed with mechanisms through which they can evade the onslaught
of host defense response. These mechanisms are discussed including diminishing the ability of
antigen presenting cells to present antigens to CD4(+) T cells; production of suppressive
cytokines; escape from fused phagosomes and inducing T cell apoptosis. The review brings out the
complexity of the host-pathogen interaction and underlines the importance of identifying the
mechanisms involved in protection, in order to design vaccine strategies and find out surrogate
markers to be measured as in vitro correlate of protective immunity. 
Immunology; Mycobacterium tuberculosis; tuberculosis