Immune System Responses against Mycobacterium tuberculosis and its Mechanisms to Escape from the Immune System

Shahrad Tafaghodi Borhani; Kaveh Vakili; Yasaman Jafari; Zahra Ghomi; Bita Zandi; Fatemeh Roozbahani; Seyedeh  Faride Alavi Rostami; Yalda Malekzadegan; Kambiz Feyzi; Fatemeh Sameni

doi:10.18502/jmb.v12i3.16610

Shahrad Tafaghodi Borhani Department of Biology, Mashhad Branch, Islamic Azad University, Mashhad, Iran.
Kaveh Vakili Health and Disease Aquatic Veterinary, Faculty of Veterinary Specialized Sciences, Islamic Azad University, Research Sciences Branch, Tehran, Iran.
Yasaman Jafari Department of Microbiology,Tehran Medical Science Branch٫Islamic Azad University,Tehran,Iran.
Zahra Ghomi Department of Microbiology, Qom Branch, Islamic Azad University, Qom, Iran
Bita Zandi Department of Microbiology, School of Medicine،Golestan University of Medical Sciences, Gorgan, Iran.
Fatemeh Roozbahani Department of Microbiology and Virology, Faculty of Medicine, Mazandaran University of Medical Sciences, Sari, Iran
Seyedeh Faride Alavi Rostami Department of Microbiology, Faculty of Biological Sciences, Islamic Azad University Tehran-North Branch, Tehran, Iran.
Yalda Malekzadegan Department of Microbiology, Saveh University of Medical Sciences, Saveh, Iran.
Kambiz Feyzi Student Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran.
Fatemeh Sameni Department of Microbiology, Faculty of Medicine, Shahed University, Tehran, Iran.

DOI: https://doi.org/10.18502/jmb.v12i3.16610

Keywords: Apoptosis, Immune system, Mycobacterium tuberculosis, Oxidative stress.

Abstract

Background: Mycobacterium tuberculosis (MTB) employs a variety of strategies to evade the host immune response, enabling its persistence and the development of tuberculosis. These evasion tactics involve thwarting lysosome formation, manipulating intracellular pH, and disrupting apoptosis and autophagy processes within host cells. Specifically, MTB interferes with lysosome acidification by modulating calcium ions (Ca2+), iron ions, and hydrogen ions (H+ ), creating an optimal environment for its survival within host cells. Furthermore, MTB inhibits host cell apoptosis and autophagy, critical defense mechanisms against intracellular pathogens. Understanding these immunological escape mechanisms is paramount for developing effective tuberculosis therapies. Future research should focus on targeting MTB evasion strategies to pave the way for innovative tuberculosis treatments.

Conclusion: There is still a long road ahead of us to understand the immunological escape mechanism used by MTB. Over the past 50 years, numerous studies have looked into the immune response and the pathogenic processes of MTB.