Abstract
Tuberculosis is a devastating disease causing high mortality all over the world, especially in the developing countries. Mycobacterium tuberculosis (M. tb) is the causative agent of tuberculosis which replicates in the intracellular environment of host macrophages. Although the host immune system is capable of completely eliminating the pathogen, co-evolution of M. tb with humans has resulted in its ability to hijack the host innate and adaptive immune systems in numerous ways. Limited recent progress has been made in the understanding of M. tb immune escape mechanisms, hence exploration of survival strategies of M. tb has been critically reviewed with an insight into understanding its pathogenesis. We summarized the recent studies regarding the modulation of innate immune response, adaptive immune response, epigenetics and the role of miRNA. All of these advancements suggest that M. tb is well-familiarize with the host immune system and possess the ability to hijack it for intracellular survival.
Highlights
Tuberculosis (TB) is described in almost all of the recorded history of humanity (Comas et al, 2013)
While infecting macrophages and dendritic cells (DCs), M. tb hijacks them for its survival and dissemination
M. tb is recognized by macrophages through pattern recognition receptors (PRRs) which include; Toll-like receptors (TLR-2, TLR-4, TLR-9), NOD-like receptors (NLR), and C-type lectin receptor (CLR) (Mortaz et al, 2015)
Summary
Tuberculosis (TB) is described in almost all of the recorded history of humanity (Comas et al, 2013). M. tb survives and replicates within the acidic environment of lysosome by engulfment in macrophages via Fcɤ receptors (Levitte et al, 2016) and Rv3671c (MarP: membrane serine protease), an acid endurance and virulence providing factor (Levitte et al, 2016) Another host factor, which is an immunosuppressive, non-classical, and class Ib molecule, is Human Leukocyte Antigen-G (HLA-G). To limit the iron acquisition by M. tb, the host cell produces natural resistance-associated macrophage protein 1 (Nramp1), which inhibits the transport of iron to the phagosome to restrict pathogen survival (Johnson and Wessling-Resnick, 2012). WhiB3 regulates virulence-associated lipids, such as sulfolipids, diacyltrehaloses, and polyacyltrehaloses, all of which stimulate both higher pro- and anti-inflammatory cytokine levels and function in maintaining reduction-oxidation (redox) (Zheng et al, 2012) These proteins aid in the survival of M. tb by retaining redox potential in the face of ROS and NOS. These refolded proteins demonstrate a reactive response in the latently-infected TB patient (Taylor et al, 2012)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
