Recombinant human Soluble TNF Receptor II protein

Supplementary information

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

Soluble TNF Receptor II also known as TNFRSF1B or CD120b acts as a decoy receptor that binds with tumor necrosis factor-alpha (TNF-α) in the serum and extracellular space. It has a molecular mass of approximately 75 kDa. This receptor is expressed in various tissues including the immune cells and plays a role in regulating inflammatory responses. By binding TNF-α Soluble TNF Receptor II prevents TNF-α from interacting with cell surface receptors modulating its inflammatory effects.

Biological function summary

Soluble TNF Receptor II modulates inflammation and immune response. It is a part of the TNF receptor superfamily and can take part in forming a receptor-ligand complex with TNF-α impacting the downstream signaling. This receptor acts to neutralize TNF-α activity by preventing its engagement with pro-inflammatory receptors on cell surfaces. Apart from its inhibitory role it also assists in the clearance of TNF-α from the circulation managing excess TNF-α levels in the body.

Pathways

Soluble TNF Receptor II is dominant in the TNF signaling pathway and the NF-κB pathway. These pathways manage immune response cell survival and apoptosis. TNFR1 another receptor in the TNF family plays a related role in the TNF signaling pathway and often collaborates with Soluble TNF Receptor II to regulate balance between cell death and cell survival. The complex formed by Soluble TNF Receptor II and TNF-α diminishes excessive inflammation by reducing active TNF-α available for binding with TNFR1.

Soluble TNF Receptor II holds significance in rheumatoid arthritis and inflammatory bowel disease. Its presence modifies the course of these diseases by modulating the levels and effects of TNF-α. The inhibition of TNF-α-driven inflammation through interaction with Soluble TNF Receptor II can reduce tissue damage and improve symptoms. In these contexts it shows links with TNF-α which is a well-known mediator of inflammation and plays a role in the pathophysiology of these inflammatory disorders.