Abstract
Tuberculosis (TB) is a very contagious, chronic disease caused by acid-fast bacilli that are notoriously difficult to eradicate from the host’s surroundings. For it to work, the host organism’s innate and adaptive immune systems must be intact. There are several sensors for recognising patterns: when foreign pathogens or their by-products are detected by immune cells, which then trigger an immunological response. To make the host more susceptible to infection and prime the immune system to fight off the invading virus, epigenetic modification is essential. By altering the expression of genes, it alters the host cell’s genetic makeup. Researchers have looked at the role of histone acetylation, ncRNA modification, methylation of DNA, and miRNA modification in TB pathophysiology to halt its development. While there has been a lot of study, many questions remain unanswered. In this chapter, we will go through the immunopathophysiological causes of TB, the basics of epigenetics, and how epigenetic research is now being used to understand the disease’s pathophysiology and progression.
| Original language | English |
|---|---|
| Title of host publication | Targeting Epigenetics in Inflammatory Lung Diseases |
| Publisher | Springer Nature |
| Pages | 127-144 |
| Number of pages | 18 |
| ISBN (Electronic) | 9789819947805 |
| ISBN (Print) | 9789819947799 |
| DOIs | |
| State | Published - 1 Jan 2023 |
| Externally published | Yes |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
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