Toll-like receptor 3 (TLR3) recognizes double-stranded (ds) RNA in the endosomal compartment. The antiviral role of TLR3 has been shown in different models. Moreover, dsRNA in necrotic cells can lead to activation of the TLR3 pathway.
Upon recognition of dsRNA, the TLR3 signaling cascade is initiated via recruitment of TRIF (toll/IL-1 receptor (TIR) domain–containing adaptor inducing IFN-β) and results in an antiviral and inflammatory response: Activation of IRF3 (IFN regulatory factor 3) leads to the production of type I IFNs and NF-κB signaling to the synthesis of inflammatory cytokines. Finally, immune cells such as dendritic cells and B cells are activated.
The natural ligands for TLR3 can be mimicked by TLR3 agonists like polyinosinic-polycytidylic acid (Poly (I:C)), a synthetic RNA oligoribonucleotide (ORN). Poly (I:C) hybridizes in aqueous solutions with high ionic strength and forms RNA double strands.
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