Recombinant Cynomolgus HVEM/TNFRSF14 Fc Chimera Protein

Recombinant Cynomolgus HVEM/TNFRSF14 Fc Chimera Protein Summary

Product Specifications

Product Datasheets

Carrier Free

CF stands for Carrier Free (CF). We typically add Bovine Serum Albumin (BSA) as a carrier protein to our recombinant proteins. Adding a carrier protein enhances protein stability, increases shelf-life, and allows the recombinant protein to be stored at a more dilute concentration. The carrier free version does not contain BSA.

In general, we advise purchasing the recombinant protein with BSA for use in cell or tissue culture, or as an ELISA standard. In contrast, the carrier free protein is recommended for applications, in which the presence of BSA could interfere.

Background: HVEM/TNFRSF14

HVEM (herpesvirus entry mediator), also known as TNFRSF14 and CD270, is a type I membrane protein in the TNF receptor superfamily, and it can both promote and inhibit T cell activity (1). Mature cynomolgous HVEM consists of a 171 amino acid (aa) extracellular domain (ECD) with three cysteine-rich domains (CRD), a 24 aa transmembrane segment, and a 42 aa cytoplasmic tail with a TRAF interaction domain (2, 3). Within the ECD, cynomolgous HVEM shares 88%, 54%, and 54% aa sequence identity with human, mouse, and rat HVEM, respectively. HVEM is highly expressed on naïve CD4⁺ T cells, CD8⁺ T memory cells, regulatory T cells, dendritic cells, monocytes, and neutrophils (4-8). Its expression declines during effector T cell activation but is up-regulated during Treg activation (4, 5). HVEM functions as a receptor for BTLA, CD160, LIGHT/TNFSF14, and Lymphotoxin-a (4, 9-12). Ligation of HVEM by LIGHT triggers T cell, monocyte, and neutrophil activation (8, 10) and contributes to Th1 inflammation and cardiac allograft rejection (13, 14). In contrast, HVEM binding to CD160 or BTLA suppresses T cell and dendritic cell activation (4, 7, 9, 10) and dampens intestinal inflammation (15). HVEM enhances the development of CD8⁺ T cell memory and Treg function (5, 6). It is additionally expressed on intestinal epithelial cells, where its binding by intraepithelial lymphocyte (IEL) expressed CD160 promotes epitheilal integrity and host defense (16). The herpesvirus envelope glycoprotein gD, which binds HVEM to initiate membrane fusion, can antagonize both BTLA and LIGHT binding (2, 9, 11).

Related Research Areas

• B Cell Development and Differentiation
• Co-stimulatory and Co-inhibitory Molecules
• Monocyte Markers
• Regulation of Apoptosis by TNF Superfamily Members
• Regulation of Natural Killer Cell Co-stimulation by TNF Superfamily Members
• Regulation of T Cell Co-stimulation by TNF Superfamily Members
• Search Immune Checkpoint Targets
• TNF Superfamily
• TNF Superfamily Receptors