Decoy receptor 3

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Decoy Receptor 3 (DcR3), also known as TNFRSF6B, is a human protein encoded by the TNFRSF6B gene. It is a member of the tumor necrosis factor receptor superfamily (TNFRSF) and plays a crucial role in the regulation of the immune system and inflammation.

Structure[edit | edit source]

DcR3 is a soluble protein that lacks a transmembrane domain, which is a characteristic feature of most members of the TNFRSF. The protein is composed of 300 amino acids and has a molecular weight of approximately 35 kDa. It contains four cysteine-rich domains, which are typical of the extracellular domains of the TNFRSF.

Function[edit | edit source]

DcR3 functions as a decoy receptor, binding to specific ligands and preventing them from interacting with their corresponding functional receptors. This mechanism is used by the body to regulate the activity of various cytokines, which are important mediators of immune and inflammatory responses. DcR3 has been shown to bind to three ligands: Fas ligand (FasL), LIGHT, and TL1A.

Fas Ligand[edit | edit source]

Fas ligand (FasL) is a type of cell death inducing ligand. By binding to FasL, DcR3 prevents it from interacting with its receptor, Fas, thereby inhibiting FasL-induced apoptosis.

LIGHT[edit | edit source]

LIGHT is a cytokine that plays a role in the regulation of cell proliferation and cell death. DcR3 binds to LIGHT and prevents it from interacting with its receptors, HVEM and LTβR, thereby modulating the activity of LIGHT.

TL1A[edit | edit source]

TL1A is a cytokine that is involved in the regulation of immune responses. DcR3 binds to TL1A and prevents it from interacting with its receptor, DR3, thereby regulating the activity of TL1A.

Clinical Significance[edit | edit source]

DcR3 has been implicated in various diseases, including cancer, autoimmune diseases, and inflammatory diseases. It has been found to be overexpressed in many types of cancer, and its expression level has been correlated with disease progression and prognosis. In autoimmune and inflammatory diseases, DcR3 has been shown to modulate immune responses and inflammation, suggesting a potential role in the pathogenesis of these diseases.

See Also[edit | edit source]

References[edit | edit source]



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Contributors: Prab R. Tumpati, MD