Toll-like receptor 3 and Toll-like receptor 4 (TLR3, TLR4)

Toll-like receptors, especially TLR3 and TLR4, are transmembrane pattern recognition receptors that detect pathogenic molecules and initiate powerful innate immune responses, including the production of interferon beta (IFN-β)[2][4]. TLR3 recognizes double-stranded RNA, mainly of viral origin, and signals exclusively through the TRIF adaptor, leading to IRF3/7 activation and robust IFN-β production[2]. TLR4 recognizes bacterial lipopolysaccharide (LPS) and signals through both MyD88-dependent and TRIF-dependent pathways; the latter is critical for IFN-β induction[1][4]. Modulation of TLR signaling has implications for infectious diseases, cancer, and autoimmune conditions, making TLR3 and TLR4 important therapeutic targets. If structure is required, select Toll-like receptor 3 (TLR3) or Toll-like receptor 4 (TLR4) as the canonical targets mediating IFN-β production[2][4]. The phrase "Toll-like receptors mediating IFN-β production" is not a proper canonical name, but a functional description; the correct structured approach would be to specify the individual TLRs involved in the pathway.

Other names

Toll-like receptor 3 (TLR3)Toll-like receptor 4 (TLR4)TLR family (collective reference)Pattern recognition receptor (functional family)

Agonism: Activates receptor to induce IFN-β and other type I interferons for antiviral/immune modulation. Antagonism: Inhibits receptor to suppress excessive immune/inflammatory response (potentially reduce cytokine storm).