Toll-like receptor 3 (TLR3) is a key component of innate and adaptive immunity. TLRs (Toll-like receptors) control host immune response against pathogens through recognition of molecular patterns specific to microorganisms. TLR3 is a nucleotide-sensing TLR which is activated by double-stranded RNA, a sign of viral infection [, , , , , ]. TLR3 assembles on dsRNA as stable dimers and the minimal signaling unit is one TLR3 dimer []. Most TLRs signal through the MyD88-dependent pathway. However, TLR3 utilises a MyD88-independent pathway. TLR3 induces type I interferon (IFN), inflammatory cytokine/chemokine production, and dendritic cell (DC) maturation via the adaptor protein TICAM-1 (also called TRIF) [].
TIR domain-containing adapter molecule 1 (TICAM1) is involved in innate immunity against invading pathogens. It is an adapter used by TLR3 and TLR4 (through TICAM2) to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis [, ].
Toll-like receptor (TLR) 3 is an endosomal TLR that mediates immune responses against viral infections upon activation by its ligand double-stranded RNA, a replication intermediate of most viruses. TLR3 is expressed widely in the body and activates both the innate and adaptive immune systems []. This entry represents the Toll-like receptor 3 trans-membrane domain which has been shown to form dimers and trimers with different surfaces for helix-helix interaction [].
