Toll-like receptor 2 (TLR2), Toll-like receptor 3 (TLR3), Toll-like receptor 4 (TLR4), Toll-like receptor 7 (TLR7), and Toll-like receptor 9 (TLR9) (TLR2/3/4/7/9)

Toll-like receptors (TLRs) 2, 3, 4, 7, and 9 are a specific subset of pattern recognition receptors (PRRs) that play a fundamental role in the innate immune system by detecting pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) (UniProt P49768, O15455, O00206, Q9NYK1, Q9NR96). TLR2 and TLR4 are primarily expressed on the cell surface, where they recognize bacterial components such as lipoproteins and lipopolysaccharides, respectively (NIH). In contrast, TLR3, TLR7, and TLR9 are localized within endosomal compartments to sense viral and bacterial nucleic acids, including double-stranded RNA, single-stranded RNA, and unmethylated CpG DNA (NIH). Activation of these receptors triggers intracellular signaling cascades via adapter proteins like MyD88 and TRIF, culminating in the production of pro-inflammatory cytokines and type I interferons (Frontiers in Immunology). These receptors are significant therapeutic targets; agonists like imiquimod and CpG oligonucleotides are used as vaccine adjuvants and cancer immunotherapies to stimulate immune responses, while antagonists like eritoran have been investigated to mitigate excessive inflammation in conditions such as sepsis and autoimmune diseases (NIH, ResearchGate). However, therapeutic modulation of these pathways carries risks, most notably the potential for inducing cytokine release syndrome or systemic autoimmunity (Frontiers in Immunology).

Other names

TLR2TLR3TLR4TLR7TLR9CD282CD283CD284CD287CD289Toll-like receptor familyTIL4TIL1

Agonism of TLRs stimulates the innate immune system to produce cytokines and interferons, enhancing vaccine efficacy and anti-tumor immunity; Antagonism of TLRs inhibits these pathways to treat inflammatory disorders and sepsis.