Bag it, tag it: ubiquitin ligases and host resistance to Mycobacterium tuberculosis

Infection with Mycobacterium tuberculosis (Mtb), the etiological agent of tuberculosis (TB), remains a significant global epidemic. Host resistance to Mtb depends on both adaptive and innate immunity mechanisms, including development of antigen-specific CD4 and CD8 T cells, production of inflammatory cytokines, bacterial phagocytosis and destruction within phagolysosomes, host cell apoptosis, and autophagy. A key regulatory mechanism in innate immunity is the attachment of the small protein ubiquitin to protein and lipid targets by the enzymatic activity of ubiquitin ligases. Here, we summarize the latest advances on the role of ubiquitination and ubiquitin ligases in host immunity against Mtb, with a focus on innate immunity signaling, inflammation, and antimicrobial autophagy. Understanding how ubiquitin ligases mediate immunity to Mtb, and the specific substrates of distinct ubiquitin ligases in the context of Mtb infection, could facilitate development of new host-directed antimicrobials.

Automated summary

This article summarizes the latest advances on the role of ubiquitination and ubiquitin ligases in host immunity against Mycobacterium tuberculosis infection. It focuses on innate immunity signaling, inflammation, and antimicrobial autophagy. Understanding the mechanisms of ubiquitin ligases in mediating immunity to Mtb could aid in the development of new host-directed antimicrobials.