TLR3, Human, mAb TLR3.7

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The monoclonal antibody TLR3.7 recognizes the 116 kDa human Toll-like receptor 3 (TLR3, CD283).Toll-like receptors (TLRs) are highly conserved from Drosophila to humans and share structural andfunctional similarities. TLRs constitute of a family of pattern recognition receptors (PRRs) that mediatecellular responses to a large variety of pathogens (viruses, bacteria, and parasites) by specificrecognition of so-called ‘pathogen-associated molecular patterns’. Activation of TLRs, a family of atleast 11 different members that function either as homo- or heterodimers, leads to activation of NFκBdependentand IFN-regulatory factor-dependent signaling pathways. TLRs have a central role ininnate immunity and are also required for the development of an adaptive immune response. TLRsare expressed by various cells of the immune system, such as macrophages and dendritic cells. TLRsare class I receptors, with a single α-helix that spans the cell membrane. They recognize and respondto molecules derived from bacterial, viral and fungal pathogens, such as lipopolysaccharide (LPS)from the outer membrane of Gram negative bacteria, peptidoglycan fragments from bacterial cell wallsand single-stranded and double-stranded RNA from viruses.Some forms of RNA and DNA from pathogens exhibit immutable features that distinguish them fromnucleic acids of higher organisms. For example, dsRNA, is a common intermediate of viral replicationand a potent indicator of infection. Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNAand its synthetic analog polyriboinosinic:polyribocytidylic acid (poly(I:C)). TLR3 is normally located inacidic endosomes where its luminal ectodomain (ECD) encounters dsRNA and induces type Iinterferon (IFN), inflammatory cytokine/chemokine production and dendritic cell (DC) maturation viathe adaptor protein TICAM-1 (also called TRIF). Based on the different subcellular localization ofcytosolic RNA receptors and TLR3, these receptors seem to play distinct roles in anti-viral immuneresponses.