Toll-like receptor on dendritic cell (TLR (on DC))

Toll-like receptors (TLRs) are a family of single-pass transmembrane pattern recognition receptors expressed on dendritic cells and other immune cells. They recognize pathogen-associated molecular patterns (PAMPs) such as bacterial lipopolysaccharide (LPS; TLR4), flagellin (TLR5), double-stranded RNA (TLR3), and unmethylated CpG DNA (TLR9), and danger-associated molecular patterns (DAMPs) from host tissue. TLR activation on dendritic cells initiates signaling cascades (e.g., MyD88-dependent, TRIF-dependent) that induce the maturation of dendritic cells, upregulation of costimulatory molecules (CD80/86/40), cytokine production (IL-6, IL-12, TNF-α, type I IFN), and efficient presentation of antigens to T cells, bridging innate and adaptive immunity. TLRs are central to responses to infection, inflammation, cancer, and are targets for drugs and vaccine adjuvants. Genetic variants in TLRs influence susceptibility to diseases such as cancer and inflammatory disorders. Overactivation or dysregulation can cause autoimmunity or pathological inflammation.

Other names

Pattern recognition receptor (PRR) familyTLRsTLR1TLR2TLR3TLR4TLR5TLR6TLR7TLR8TLR9

Agonists: Bind TLRs to activate downstream signaling (e.g., NF-κB activation), leading to cytokine secretion, dendritic cell maturation, antigen presentation, and enhanced immune response (sometimes used as vaccine adjuvants). Antagonists: Block activation to suppress unwanted inflammation (e.g., sepsis, autoimmune disease).