Interconnection of Mycobacterium tuberculosis with host immune system

Precise estimation of development of active tuberculosis (TB) infection from a latent Mycobacterium tuberculosis H 37 Rv (MTB) infection within host body signifies an indefinable and serious objective.Most of the infected individuals with excellent immune system are also at risk due to diverse local environmental and systemic factors.Therefore, it becomes mandatory to have a balance between pro and anti-immune regulators to work efficiently in optimized manner.This study thus signifies some essential factors involved in maintaining this balance and rescue host cellular environment from MTB infection.Inside host, MTB develops effective survival strategies, such as hampering of lysosome-phagosome fusion, hampering of phagosome acidification by a secretary protein phosphatase PtpA that binds to H subunit of V-ATPase to block V-ATPase transportation towards phagosome membrane, recruitment of TACO protein on phagosomal membrane to escape their transportation to lysosome.Bacterial infected cell undergoing apoptosis release ATP, UTP, LPC, S1P and several chemokines that intervene signaling of "find me" signal.Eventually, a balance between all these immunological factors must be set for optimized functioning of immune system against MTB.In this review we have elaborated various balancing mechanisms among pro and anti-inflammatory immune components that raise this disease from latent to active form.Through a brief and complete evaluation of different types of immune components that take part in host defense, we aimed to highlight the review with recent documented literatures to have a better and precise understanding of this disease.In conclusion, this review abridges various defensive strategies that moderate the distinct capability to fight MTB infection.