TY - JOUR
AU - Flavell, Richard A.
AB - Toll-like receptors (TLRs) are a family of innate immune-recognition receptors that recognize molecular patterns associated with microbial pathogens, and induce antimicrobial immune responses
1,2
. Double-stranded RNA (dsRNA) is a molecular pattern associated with viral infection, because it is produced by most viruses at some point during their replication
3
. Here we show that mammalian TLR3 recognizes dsRNA, and that activation of the receptor induces the activation of NF-κB and the production of type I interferons (IFNs). TLR3-deficient (TLR3-/-) mice showed reduced responses to polyinosine–polycytidylic acid (poly(I:C)), resistance to the lethal effect of poly(I:C) when sensitized with d-galactosamine (d-GalN), and reduced production of inflammatory cytokines. MyD88 is an adaptor protein that is shared by all the known TLRs
1
. When activated by poly(I:C), TLR3 induces cytokine production through a signalling pathway dependent on MyD88. Moreover, poly(I:C) can induce activation of NF-κB and mitogen-activated protein (MAP) kinases independently of MyD88, and cause dendritic cells to mature.
TI - Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3
JF - Nature
DO - 10.1038/35099560
DA - 2001-10-18
UR - https://www.deepdyve.com/lp/springer-journals/recognition-of-double-stranded-rna-and-activation-of-nf-b-by-toll-like-BsNmJpBoou
SP - 732
EP - 738
VL - 413
IS - 6857
DP - DeepDyve
ER -