Toll-Like Receptor Signaling in Immune Modulation
Summary
Toll-like receptors (TLRs) are a family of pattern recognition receptors that detect conserved microbial motifs and endogenous danger signals, orchestrating the first line of host defence. Upon ligand binding, TLRs recruit adaptor proteins such as MyD88 or TRIF to activate downstream kinases and transcription factors, including NF-κB and interferon regulatory factors, leading to production of cytokines, chemokines and type I interferons. This core signalling axis not only drives acute inflammation against pathogens but also shapes adaptive immunity by influencing dendritic cell maturation and T cell priming. Fine-tuning of TLR responses is achieved through accessory molecules, ubiquitin-mediated regulation and negative regulators, which prevent uncontrolled inflammation. Dysregulation of TLR signalling underlies a range of conditions, from sepsis and autoimmune disease to cardiovascular remodelling, and TLRs remain attractive targets for vaccine adjuvants and immunotherapies.
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Toll-Like Receptor Signaling in Immune Modulation publication trend
The graph below shows the total number of articles in toll-like receptor signaling in immune modulation across all publications each year (not limited to Nature Index journals).
Technical terms
Toll-Like Receptor (TLR): A membrane receptor that recognises microbial or host-derived patterns to initiate immune signalling.
Pathogen-Associated Molecular Pattern (PAMP): Conserved microbial structure recognised by TLRs to trigger innate immunity.
Damage-Associated Molecular Pattern (DAMP): Endogenous molecule released from damaged cells that activates TLR-mediated inflammation.
Accessory molecule: A co-receptor or chaperone that modulates TLR ligand binding or downstream signal transduction.
Adjuvant: An agent that enhances immune responses to an antigen, often via engagement of TLRs.
References
- A Novel Gene Delivery Vector of Agonistic Anti-Radioprotective 105 Expressed on Cell Membranes Shows Adjuvant Effect for DNA Immunization Against Influenza. Frontiers in Immunology (2020).
- Toll-like receptors in cardiac hypertrophy. Frontiers in Cardiovascular Medicine (2023).
- TLR Accessory Molecule RP105 (CD180) Is Involved in Post-Interventional Vascular Remodeling and Soluble RP105 Modulates Neointima Formation. PLOS ONE (2013).
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