Epigenetic regulatory landscape of innate immune cells in tuberculosis (Review)

This review presents an analysis of current research on the role of epigenetic mechanisms in regulating gene expression, which is fundamental to key functions of innate immunity in tuberculosis. Tuberculosis (TB), caused by Mycobacterium tuberculosis, has a profound and multifaceted impact on human health. It can lead to a decline in quality of life, disability, and mortality, and is also associated with psychosocial challenges. Non-coding RNAs (ncRNAs) are extensively involved in numerous biological processes, including M. tuberculosis infection, and play a crucial role in gene regulation.  In this review, we summarise findings on ncRNAs that influence the host’s immune response to M. tuberculosis infection. Our analysis demonstrates that pathogens can exploit interactions between ncRNAs and other biomolecules to evade immune-mediated clearance mechanisms and persist within host cells for extended periods. During the interaction between M. tuberculosis and host macrophages, ncRNA expression levels undergo significant alterations, affecting the regulation of host cell metabolism, inflammatory responses, apoptosis, and autophagy. These findings provide valuable insights that could contribute to the development of novel approaches for the diagnosis and treatment of tuberculosis.