Anti-TLR4/MD2 antibody [MTS510] - Low endotoxin, Azide free

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

TLR4/MD2 also known as Toll-like receptor 4 and myeloid differentiation factor 2 acts as a critical component within the immune system. The TLR4/MD2 complex forms through the interaction between the TLR4 protein and the accessory molecule MD2 enabling recognition of lipopolysaccharides (LPS) from Gram-negative bacteria. TLR4 is a transmembrane protein expressed on various immune cells such as macrophages and dendritic cells. The molecular weight of TLR4 is approximately 96 kDa. Its localization on immune cells allows it to respond promptly to pathogens and initiate necessary immune responses.

Biological function summary

TLR4/MD2 plays a major role in the innate immune response by forming part of a receptor complex. This complex recognizes pathogen-associated molecular patterns and triggers immune signaling that results in the production of pro-inflammatory cytokines. The activation of TLR4/MD2 initiates a cascade of events that enhance the immune system’s ability to fight infections effectively. By signaling through downstream adaptor proteins like MyD88 and TRIF TLR4/MD2 mediates the activation of NF-κB and interferon-regulatory factors leading to gene expression changes and immune activation.

Pathways

The TLR4/MD2 complex aligns with critical signaling pathways involved in inflammation and immune regulation. It holds a significant position in the MyD88-dependent and TRIF-dependent pathways impacting the NF-κB signaling cascade. The interaction with proteins like MyD88 links TLR4/MD2 to the inflammatory response. These pathways reinforce TLR4/MD2's central role in modulating the immune response to protect the host from pathogens while maintaining homeostasis.

TLR4/MD2 exhibits a connection to conditions involving excessive inflammation such as sepsis and rheumatoid arthritis. In sepsis the overactivation of TLR4/MD2 leads to systemic inflammation and potential organ failure. Rheumatoid arthritis manifests chronic inflammation in part due to altered TLR4 signaling. The interaction with other proteins like TRIF is integral to understanding the mechanisms by which TLR4/MD2 contributes to these diseases. Studies target these pathways for therapeutic intervention aiming to modulate TLR4/MD2 activity to alleviate disease symptoms.