作者: Tiffany Horng , Gregory M. Barton , Richard A. Flavell , Ruslan Medzhitov
DOI: 10.1038/NATURE01180
关键词:
摘要: Mammalian Toll-like receptors (TLRs) function as sensors of infection and induce the activation innate adaptive immune responses1,2,3. Upon recognizing conserved pathogen-associated molecular products, TLRs activate host defence responses through their intracellular signalling domain, Toll/interleukin-1 receptor (TIR) downstream adaptor protein MyD88 (refs 1–3). Although members TLR interleukin-1 (IL-1) families all signal MyD88, pathways induced by individual differ. TIRAP, an in pathway, has been identified shown to TLR4 4, 5). Here we report generation mice deficient Tirap gene. TIRAP-deficient respond normally TLR5, TLR7 TLR9 ligands, well IL-1 IL-18, but have defects cytokine production nuclear factor NF-κB mitogen-activated kinases response lipopolysaccharide, a ligand for TLR4. In addition, are also impaired ligands TLR2, TLR1 TLR6. Thus, TIRAP is differentially involved family may account specificity TLRs.