TNFRSF6B Human
Description
Product Specs
Product Science Overview
TNFRSF6B acts as a decoy receptor, which means it competes with death receptors for ligand binding, thereby inhibiting apoptosis (programmed cell death) and promoting cell survival . This receptor is particularly effective in neutralizing the cytotoxic ligands TNFS14/LIGHT, TNFSF15, and TNFSF6/FASL . By doing so, it protects cells from apoptosis and can also induce angiogenesis (formation of new blood vessels) via the neutralization of TL1A .
The primary role of TNFRSF6B is to modulate immune responses and cell death pathways. It has been shown to have both “decoy” and “non-decoy” actions . The decoy action involves neutralizing the effects of TNFSF members, thereby preventing apoptosis and promoting cell survival. The non-decoy action involves modulating the activation and differentiation of immune cells such as dendritic cells (DCs) and macrophages . For instance, DcR3-treated DCs can skew T cell differentiation into a Th2 phenotype, while DcR3-treated macrophages exhibit an M2 phenotype, which is associated with tissue repair and anti-inflammatory responses .
TNFRSF6B is upregulated in various cancer cells and inflammatory tissues, making it a potential biomarker for predicting the progression of inflammatory diseases and cancer metastasis . Its expression is typically low under physiological conditions but is significantly increased in pathological conditions . This upregulation can serve as a negative feedback mechanism to suppress inflammation during inflammatory reactions. However, tumor cells can hijack this mechanism to prevent apoptosis and promote tumor growth and invasion .
Given its role in modulating immune responses and cell death pathways, TNFRSF6B has significant therapeutic potential. For inflammatory diseases, “switching on” the expression of TNFRSF6B could enhance tissue repair and suppress inflammation . Conversely, “switching off” its expression could promote tumor apoptosis and inhibit tumor growth, making it a promising target for cancer therapy .
Research on TNFRSF6B is ongoing, with studies focusing on its expression in various pathological conditions and its potential as a therapeutic target . Due to the absence of DcR3 in the mouse genome, researchers often use transgenic mice that overexpress DcR3 to study its systemic effects in vivo . Additionally, recombinant forms of TNFRSF6B, such as DcR3.Fc fusion proteins, are used to investigate its effects in vitro .
