Abstract

Our understanding of tuberculosis (TB) pathology and immunology has become extensively deeper and more refined since the identification ofMycobacterium tuberculosis(MTB) as the etiologic agent of disease by Dr. Robert Koch in 1882. A great challenge in chronic disease is to understand the complexities, mechanisms, and consequences of host interactions with pathogens. TB, caused by MTB, is a major health problem in world, with 10 million new cases diagnosed each year. Innate immunity is shown playing an important role in the host defense against the MTB, and the first step in this process is recognition of MTB by cells of the innate immune system. Several classes of pattern recognition receptors (PPRs) are involved in the recognition of MTB, including toll-like receptors (TLRs), C-type lectin receptors (CLRs), and nod-like receptors (NLRs). Among the TLR family, TLR1, TLR2, TLR4, and TLR9 and their down streams, proteins play the most prominent roles in the initiation of the immune response against MTB. Beside of TLRs signaling, recently the activation of inflammasome pathway in the pathogenesis of TB much appreciated. Knowledge about these signaling pathways is crucial for understanding the pathophysiology of TB, on one hand, and for the development of novel strategies of vaccination and treatment such as immunotherapy on the other. Given the critical role of TLRs/inflammasome signaling in innate immunity and initiation of the appropriate adaptive response, the regulation of these pathways is likely to be an important determinant of the clinical outcome of MTB infection. In this review paper we focused on the immune response, which is the recognition of MTB by inflammatory innate immune cells following infection.

Highlights

  • Despite the availability of effective and inexpensive therapy, TB is considered as one of the leading causes of death from an infectious disease worldwide [1].For long time it is believed that TB is a major public health problem in the world, with 10 million new cases diagnosed each year, causing a death toll of 2 million victims

  • These cells can lyse macrophages containing mycobacteria and are an early source of IFN-γ [31]. They might have a role in the initial, innate immune response to Mycobacterium tuberculosis (MTB), because their population is expanded by mycobacteria and mycobacterial products in tissues

  • The cytokine IL-10, which is generally secreted by TH2 cells, affects macrophages by suppressing cytokine production, and thereby downregulating TH1 cell activity and proliferation, and one study suggests that IL-10 plays a central role in enhancing the survival of MTB within macrophages [90]

Read more

Summary

Introduction

Despite the availability of effective and inexpensive therapy, TB is considered as one of the leading causes of death from an infectious disease worldwide [1]. The role of inborn variability in susceptibility to TB has been described [4]. This finding indicates that at least some individuals display an effective immune response against the MTB and that this plays an important part in determining the disease [5]. This episode in young infants known to have immature adaptive immunity suggests that the innate host defense is an important arm of antimycobacterial host defense [6]. ISRN Immunology as toll-like receptors (TLRs) or inflammasome pathways and how these receptors contribute to inflammation by signal transduction pathways

Immunology of MTB
Cellular Immunity to MTB
Role of Signal Transduction Pathways in the Pathogenesis of MBT
Findings
Conclusion and Future Research
Full Text
Published version (Free)

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 call