Toll Receptor Type 1/CD281

The mammalian host defense system is essentially regulated by highly conserved Toll-like receptor (TLR) family of proteins.  At least 13 TLRs have been identified and cloned in mammalian cells which recognize molecular products/signals from all the major classes of pathogens.  The Toll signaling to NF-Kb starts form conserved Toll-IL-1-resistance (TIR) domain, which mediated the coupling of TIR adaptor molecules (MyD88, Mal, TICAM and TRAM) and caused production of inflammatory cytokines such as IL-1, IL-6, IL-8 , TNFa, and IL-12, chemokines and costimulatory molecules such as CD40, CD80 and CD86.  In the presence of inflammatory cytokines and binding of adaptor molecule, MyD88 that binds FADD and triggers apoptosis through the caspase cascade.  TLR induced apoptosis pathway appears to be a repatoire of defence mechanism utilized by innate defense mechanism.  The constitutive expression of many human TLRs (1, 2, 4) have been shown on the surface of myeloid lineage cells by RT-PCR and use of specific monoclonal antibodies.  Upon activation of these receptors by their respective chemokines and ligands have been shown in literature on various cell lines including endothelial, epithelial and other cells.  The expression of TLR 3, 7, 8 and 9 are mainly found on endosomal lysosomal compartments.  Human TLR3 is expressed in human fibroblasts cells and TLR 9 in in-vitro derived DC cells.   There is significant evidence of TLR involvement is many systemic disorders following bacterial infection including sepsis, peridontitis, cardiac ischemia, cerebral palsy and others, understanding the TLRs involvement in these conditions will allow therapeutic interventions at the receptor level for treatment of these disorders. 

For research use only, not for diagnostic or therapeutic use.