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Immunomodulation by epigenome alterations in Mycobacterium tuberculosis infection
Kavya Gauba1, Shruti Gupta1, Jyoti Shekhawat1
1Department of Biochemistry, All India Institute of Medical Sciences, Jodhpur, 342005, India.
Mycobacterium tuberculosis (MTB) evades host immunity by altering the host epigenome. This review explores how MTB manipulates epigenetic modifications like DNA methylation and chromatin remodeling for its survival.
Area of Science:
- Immunology
- Microbiology
- Epigenetics
Background:
- Mycobacterium tuberculosis (MTB) has co-evolved with humans, developing sophisticated immune evasion strategies.
- Epigenetic modifications, including DNA methylation and chromatin remodeling, significantly influence gene expression and cellular processes.
- The role of epigenetics in disease pathogenesis is increasingly recognized, offering potential for novel diagnostic and therapeutic approaches.
Purpose of the Study:
- To review the fundamental principles of epigenetics.
- To elucidate the mechanisms by which MTB reshapes the host epigenetic landscape.
- To understand how MTB utilizes epigenetic alterations to suppress host immune responses for its survival and persistence.
Main Methods:
- This is a review article, synthesizing existing research on MTB and host epigenetics.
- Literature search and analysis of studies investigating epigenetic modifications in the context of MTB infection.
- Examination of molecular mechanisms underlying MTB-induced epigenetic changes.
Main Results:
- MTB actively modulates host gene expression through epigenetic alterations.
- Specific epigenetic mechanisms employed by MTB include DNA methylation and chromatin remodeling.
- These modifications lead to the suppression of immune responses crucial for pathogen clearance.
Conclusions:
- Epigenetic reprogramming is a key survival strategy for MTB.
- Understanding these epigenetic interactions is vital for developing new anti-TB therapies.
- Targeting host epigenetic modifications presents a promising avenue for combating tuberculosis.
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