Toll-Like Receptor Signaling in Mycobacterium tuberculosis Interactions
Summary
The interplay between Mycobacterium tuberculosis (Mtb) and the host’s innate immune system is orchestrated in large part by Toll-like receptors (TLRs), a family of transmembrane pattern recognition receptors expressed on macrophages, dendritic cells and epithelial cells. Engagement of Mtb-derived ligands such as lipoproteins, glycolipids and nucleic acids with TLR2, TLR4 and TLR9 initiates downstream signalling cascades through adaptor molecules including MyD88 and TIRAP. This leads to activation of NF-κB and MAP kinase pathways, induction of proinflammatory cytokines (for example TNF-α and IL-6) and promotion of phagosome maturation. A balanced response can drive bacterial containment and granuloma formation, whereas dysregulation may permit Mtb survival, dissemination or excessive tissue damage. Cross-talk with other innate pathways, notably inflammasomes and autophagy machinery, further refines the outcome of infection. Genetic polymorphisms in TLRs and associated adaptors affect susceptibility to active tuberculosis and treatment outcomes across global populations. Understanding the precise molecular events by which Mtb manipulates TLR signalling has given rise to host-directed therapeutic strategies aimed at reinforcing phagosomal acidification, enhancing antimicrobial effector functions and modulating inflammatory networks to improve disease resolution and reduce lung pathology.
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Toll-Like Receptor Signaling in Mycobacterium tuberculosis Interactions publication trend
The graph below shows the total number of articles in toll-like receptor signaling in mycobacterium tuberculosis interactions across all publications each year (not limited to Nature Index journals).
Technical terms
Toll-like receptor (TLR): A family of pattern recognition receptors that detect conserved microbial molecules and initiate innate immune signalling.
MyD88: An adaptor protein that links most TLRs to downstream kinases and transcription factors, driving inflammatory gene expression.
Phagosome maturation: The process by which a pathogen-containing vesicle fuses with lysosomes to create an acidic environment for microbial killing.
NF-κB: A transcription factor complex central to the expression of proinflammatory cytokines and co-stimulatory molecules.
Cish: A cytokine-inducible SH2 domain-containing protein that modulates signal transduction and impacts phagosomal trafficking.
Pattern-associated molecular pattern (PAMP): A conserved microbial structure recognised by innate receptors to trigger host defence responses.
References
- Tirap controls Mycobacterium tuberculosis phagosomal acidification. PLOS Pathogens (2023).
- TLR2 is non-redundant in the population and subpopulation responses to Mycobacterium tuberculosis in macrophages and in vivo. mSystems (2023).
- Toll-like receptor 2 (−196 to −174) del and TLR1 743 A > G gene polymorphism—a possible association with drug-resistant tuberculosis in the north Indian population. Frontiers in Microbiology (2024).
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