HVEM/TNFRSF14 Antibody (2742B) [Alexa Fluor™ Plus 647]

• Reactivity: Hu
• Clone: 2742B
• Clonality: Monoclonal
• Host: Rabbit
• Conjugate: Alexa Fluor Plus 647

HVEM/TNFRSF14 Antibody (2742B) [Alexa Fluor™ Plus 647] Summary

• Specificity: Detects human HVEM/TNFRSF14 in ELISA.
• Isotype: IgG
• Clonality: Monoclonal
• Host: Rabbit

Packaging, Storage & Formulations

• Storage: Protect from light. Do not freeze. 12 months from date of receipt, 2 to 8 °C as supplied
• Buffer: Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Alternate Names for HVEM/TNFRSF14 Antibody (2742B) [Alexa Fluor™ Plus 647]

• ATAR
• CD270 antigen
• CD270
• CD40-like protein
• Herpes virus entry mediator A
• Herpesvirus entry mediator A
• HveA
• HVEM
• HVEMTR2HVEAATAR
• LIGHTR
• TNFRSF14
• tumor necrosis factor receptor superfamily member 14
• tumor necrosis factor receptor superfamily, member 14 (herpesvirus entrymediator)
• Tumor necrosis factor receptor-like 2
• tumor necrosis factor receptor-like gene2

Background

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 human HVEM consists of a 164 amino acid (aa) extracellular domain (ECD) with three cysteine-rich domains (CRD), a 21 aa transmembrane segment, and a 60 aa cytoplasmic tail with a TRAF interaction domain (2, 3). Within the ECD, human HVEM shares 55% aa sequence identity with mouse and rat HVEM. Alternative splicing generates an additional isoform with a substitution of the N-terminal 10 amino acids including the signal peptide. 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-alpha (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).

1. del Rio, M.L. et al. (2010) J. Leukoc. Biol. 87:223.
2. Montgomery, R.I. et al. (1996) Cell 87:427.
3. Hsu, H. et al. (1997) J. Biol. Chem. 272:13471.
4. Sedy, J. R. et al. (2005) Nat. Immunol. 6:90.
5. Tao, R. et al. (2008) J. Immunol. 180:6649.
6. Steinberg, M.W. et al. (2013) PLoS One 8:e77992.
7. de Trez, C. et al. (2008) J. Immunol. 180:238.
8. Heo, S.K. et al. (2006) J. Leukoc. Biol. 79:330.
9. Gonzalez, L.C. et al. (2005) Proc. Natl. Acad Sci. USA 102:1116.
10. Cai, G. et al. (2008) Nat. Immunol. 9:176.
11. Mauri, D.N. et al. (1998) Immunity 8:21.
12. Harrop, J.A. et al. (1998) J. Biol. Chem. 273:27548.
13. Wang, J. et al. (2005) J. Immunol. 174:8173.
14. Ye, Q. et al. (2002) J. Exp. Med. 195:795.
15. Steinberg, M.W. et al. (2008) J. Exp. Med. 205:1463.
16. Shui, J.W. et al. (2012) Nature 488:222.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.