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Full Version: Innate Immune Effectors in Mycobacterial Infection
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Innate Immune Effectors in Mycobacterial Infection
TB causes more deaths than any other infectious agent in the world.
TB kills nearly 2 million people per year.
The risk of disease is also increased.
Mycobacterium Tuberculosis
Infection is acquired through the inhalation of aerosolized infectious particles.
Mtb invades alveolar macrophages to enter into the host .
Host defense against Mtb is mediated by a combination of innate and adaptive immune responses.
Identification and characterization of pattern recognition receptors (PRRs).
Involvement of PRRs other than TLRs.
PRR-independent mechanisms for mycobacterial killing, such as autophagy.
Toll-Like Receptors in Mycobacterial Infection
Non-TLRs in Mycobacterial Infection
Effectors for Mycobacterial Killing
Autophagy in Mycobacterial Infection
Human Genetics in Tuberculosis
Polymorphisms of the SLC11A1 gene are associated with tuberculosis.
TLR2 polymorphism influences the susceptibility of Mtb infection .
VDR polymorphisms have also been implicated in the susceptibility of Mtb infection.
The emergence of multidrug-resistant Mtb is now a major public health problem all over the world.
More precise understanding of the innate immune response to Mtb will pave the way for the development of an effective drug that targets the host innate immunity for the treatment of tuberculosis