Monoclonal antibody mT2.4 reacts with mouse Toll-like receptor 2 (TLR2, CD282). Toll-like receptors (TLR) are highly conserved throughout evolution and have been implicated in the innate defense to many pathogens. In Drosophila toll is required for the anti-fungal response, while the related 18-wheeler is involved in antibacterial defenses. In mammals, TLR identified as type I transmembrane signaling receptors with pattern recognition capabilities, have been implicated in the innate host defense to pathogens. TLR2 has been identified as a receptor that is central to the innate immune response to lipoproteins of Gram-negative bacteria, several whole Gram-positive bacteria, as well as a receptor for peptidoglycan and lipoteichoic acid and other bacterial cell membrane products. A functional interaction between TLR2 and TLR6 in the cellular response to various bacterial products has been discovered. The currently accepted paradigm regards TLR2 as an essential receptor for many eubacterial cell wall components, including lipoproteins and peptidoglycan. Bacterial species as diverse as mycobacteria, spirochetes, mycoplasma, Staphylococcus aureus, and Streptococcus pneumoniae have all been shown to mediate cellular activation via TLR2. The monoclonal antibody mT2.4 inhibits murine TLR2-mediated cell activation. It masks the lipopeptide binding site in the recombinant extracellular domain of TLR2 (TLR2ECD) and does not hinder the receptor complex formation. The antibody reacts with the native TLR2 protein and not with denatured TLR2 protein . Furthermore the antibody stains overexpressed, as well as endogenous cell surface- and intracellular mouse TLR2.
Flow cytometry, Frozen sections, Functional studies, Immuno assays, Paraffin sections
For immunohistology and flow cytometry dilutions to be used depend on detection system applied. It is recommended that users test the reagent and determine their own optimal dilutions. The typical starting working dilution is 1:50. For neutralization of biological activity in vitro dilutions have to be made according to the amounts of TLR2 (CD282) to be inactivated.