TLR4/MD-2 Complex Monoclonal Antibody (MTS510), eBioscience™, Invitrogen™

Description

• The MTS510 MAb reacts with the mouse Toll-like receptor 4 (TLR4)/MD-2 complex
• At least ten members of the Toll family have been identified
• This family of type I transmembrane proteins is characterized by an extracellular domain with leucine-rich repeats and a cytoplasmic domain with homology to the type I IL-1 receptor
• Two of these receptors, TLR2 and TLR4, are pattern recognition receptors and signaling molecules in response to bacterial lipoproteins and have been implicated in innate immunity and inflammation
• TLR4 physically associates with MD-2, and together with CD14, this complex is responsible for LPS recognition and signaling
• In the mouse, TLR4 is expressed by thioglycolate-elicited peritoneal macrophages
• Incubation of peritoneal macrophages with LPS results in down regulation of surface TLR4/MD-2
• The TLR4 gene is defective in C3H/HeJ and C57BL/10ScCr mice, both of which have been well characterized as hyporesponders to LPS
• The MTS510 MAb co-immunoprecipitates MD-2 (∽30 kDa) and TLR4 (∽100 kDa), and preferentially reacts with TLR4 that is associated with MD-2
• In comparison, binding of the UT41 MAb occurs with and without formation of the TLR4/MD-2 complex
• Please contact eBioscience Technical Support for further information
• MD-2 is a member of the Toll/interleukin-1 receptor (TIR) family, a group of proteins that include the Toll-like receptors (TLRs)
• TLRs are signaling molecules that recognize different pathogen-associated molecular patterns (PAMPs) and serve as an important link between the innate and adaptive immune responses
• TLR4, the major signaling receptor for lipopolysaccharide (LPS), requires the binding of MD-2 to its extracellular region for maximal response to LPS
• The specificity of this response is determined by the species of MD-2; e.g., human MD-2 transfected into mouse cells can cause mouse TLR4 to react to LPS analogs that are normally antagonistic to human but not mouse TLR4.