>95%, by SDS-PAGE visualized with Silver Staining and quantitative densitometry by Coomassie® Blue Staining.
<0.10 EU per 1 μg of the protein by the LAL method.
Measured by its binding ability in a functional ELISA. When Recombinant Cynomolgus Monkey HVEM/TNFRSF14 Fc Chimera is coated at 2 µg/mL (100 μL/well), biotinylated recombinant mouse BTLA Fc Chimera binds with a typical ED50 of 150-750 ng/mL.
WhenRecombinant Cymomologus HVEM/TNFRSF14 Fc Chimera (Catalog # 9197-HV) is coated at2 μg/mL, Recombinant Biotinylated Mouse BTLA Fc Chimera binds with a typicalED50 of 150-750 ng/mL.
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).
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