Anti-TLR6 (Clone: ABM1B50)

TLR6 (Toll-Like Receptors 6) is a member of the TLR (Toll-like receptor) family that plays a fundamental role in pathogen recognition and activation of innate immunity. TLR6 forms heterodimers with TLR1 and TLR2, which is the initial step in a cascade of events leading to significant innate immune responses, development of adaptive immunity to pathogens and protection from immune sequelae related to infection with these pathogens. TLR2 in co-operation with TLR6 trigger inflammatory responses via activation of NF-kappaB, which regulates the transcription of inflammatory molecules. TLR6 has emerged as the most potent activator for ZNPs (Zinc Oxide Nanoparticles)-induced inflammatory responses. Upon silencing, TLR6 significantly inhibited the pro-inflammatory cytokine levels, reactive nitrogen species generation and inducible nitric oxide synthase expression. Protein function: Participates in the innate immune response to Gram- positive bacteria and fungi. Specifically recognizes diacylated and, to a lesser extent, triacylated lipopeptides (PubMed:20037584). In response to diacylated lipopeptides, forms the activation cluster TLR2:TLR6:CD14:CD36, this cluster triggers signaling from the cell surface and subsequently is targeted to the Golgi in a lipid-raft dependent pathway (PubMed:16880211). Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Recognizes mycoplasmal macrophage-activating lipopeptide-2kD (MALP-2), soluble tuberculosis factor (STF), phenol-soluble modulin (PSM) and B.burgdorferi outer surface protein A lipoprotein (OspA-L) cooperatively with TLR2 (PubMed:11441107). In complex with TLR4, promotes sterile inflammation in monocytes/macrophages in response to oxidized low-density lipoprotein (oxLDL) or amyloid-beta 42. In this context, the initial signal is provided by oxLDL- or amyloid- beta 42-binding to CD36. This event induces the formation of a heterodimer of TLR4 and TLR6, which is rapidly internalized and triggers inflammatory response, leading to the NF-kappa-B- dependent production of CXCL1, CXCL2 and CCL9 cytokines, via MYD88 signaling pathway, and CCL5 cytokine, via TICAM1 signaling pathway, as well as IL1B secretion (PubMed:11441107, PubMed:20037584). [The UniProt Consortium]