Toll-like receptors (TLRs) are a central element in the innate immune response and one of the key factors involved in recognizing and defending against invading pathogens. They are transmembrane receptors that can be localized either to the cell surface or to endosomal vesicles, and belong to the pattern recognition receptor (PRR) family along with the mannose (CD206), NOD, and NALP receptors. Since they are involved in self- vs. non-self identification, they are also thought to be involved in autoimmune disease.
Initially identified in Drosophila, there are currently 13 known homologs of Toll, 10 of which are expressed in mammals. TLRs can be found either as individual transmembrane units, or in pairs and along with a range of accessory signaling molecules. Most TLR signaling occurs through a TIR domain-containing adaptor, such as MyD88, TRIF, and TRAM. Downstream signaling regulates inflammatory cytokine production and co-stimulatory receptor expression via the NF-kappaB pathway.
In addition, antibodies directed against proteins in the TLR signaling cascade are also available. These include both members of the MyD88 dependent pathway, such as: MyD88, TIRAP, IRAK1, and IRAK4, as well as TRIF from the MyD88 independent pathway.