• Species Reactivity

  Mouse

• Specificity

  Detects mouse HVEM/TNFRSF14 in direct ELISAs. Stains mouse HVEM/TNFRSF14 transfectants but not irrelevant transfectants in flow cytometry.    
   

• Source

  Recombinant Monoclonal Rabbit IgG Clone # 2024B

• Purification

  Protein A or G purified from cell culture supernatant

• Immunogen

  Chinese hamster ovary cell line CHO-derived recombinant mouse HVEM/TNFRSF14    
  Gln39-Val207    
  Accession # NP_849262

• Formulation

  Supplied in a saline solution containing BSA and Sodium Azide.

• Label

  Phycoerythrin

Applications

• 
  

  Recommended    
  Concentration

  Sample

• Flow Cytometry

  0.25 µg/10    ⁶ cells

  See below

• 
  

Please Note: Optimal dilutions should be determined by each laboratory for each application.  are available in the Technical Information section on our website.

Data Examples

Preparation and Storage

• Shipping

  The product is shipped with polar packs. Upon receipt, store it immediately at the temperature recommended below.

• Stability & Storage

  Protect from light.    Do not freeze.    

• 12 months from date of receipt, 2 to 8 °C as supplied.

Background: HVEM/TNFRSF14

HVEM (Herpesvirus Entry Mediator) is a type I membrane protein that is TNF receptor superfamily member 14 (TNFRSF14) (1). The mouse HVEM cDNA encodes a 275 amino acid (aa) protein. It contains a 36 aa signal peptide, a 170 aa extracellular domain with three cysteine rich domains (CRD), a 24 aa transmembrane region and a 45 aa cytoplasmic tail with a TRAF interaction domain (1). HVEM expression is highest on naïve, memory and regulatory T cells, but declines during T cell activation (2, 3). It is present at low levels on most resting leukocytes (4). HVEM is a receptor for the IGSF member BTLA (B and T Lymphocyte Attenuator), CD160, and the TNF family ligand LIGHT (2, 9). HVEM and BTLA are constitutively expressed on T cells, while LIGHT is generally considered to be inducible upon TCR activation. In the absence of activation, HVEM and BTLA interact monomerically, either in cis, or in trans. A same cell (or cis) interaction likely promotes general cell survival, while a between cell (or trans) interaction promotes a state of lymphocyte inactivity through the BTLA cytoplasmic domain. Following T cell activation, LIGHT appears and disrupts existing HVEM-BTLA bonds. A LIGHT-HVEM trimer now forms in trans, initiating HVEM-mediated NF kappa B signaling and a proinflammatory response (10). BTLA and LIGHT interactions are not mutually exclusive, but BTLA appears dominant (4, 6, 7). The herpesvirus envelope glycoprotein gD, which binds HVEM CRD1 to initiate membrane fusion, can antagonize both BTLA and LIGHT binding (1, 6, 7, 9). Human, but not mouse, HVEM can also bind lymphotoxin a within CRD2 3 (9, 11). Graft‑vs‑host disease and Th1 type intestinal inflammation can be ameliorated by interrupting T cell LIGHT/HVEM interactions, while disruption of BTLA/HVEM interaction promotes intestinal inflammation (12-14). Mouse HVEM ECD shares 89% and 53% aa identity with rat and human HVEM, respectively. Mouse HVEM can recognize human BTLA and LIGHT, but human HVEM does not recognize mouse ligands (2, 11).

• References:

1. Hsu, H. et al. (1997) J. Biol. Chem. 272:13471.

2. Sedy, J.R. et al. (2005) Nat. Immunol. 6:90.

3. Tao, R. et al. (2008) J. Immunol. 180:6649.

4. Wang, Y. et al. (2005) J. Clin. Invest. 115:711.

5. Nelson, C.A. et al. (2008) J. Immunol. 180:940.

6. Gonzales, L.C. et al. (2005) Proc. Natl. Acad Sci. USA 102:1116.

7. Compaan, D.M. et al. (2005) J. Biol. Chem. 280:39553.

8. Cai, G. et al. (2008) Nat. Immunol. 9:176.

9. Mauri, D.N. et al. (1998) Immunity 8:21.

10. Ware, C.F. (2008) Immunol. Rev. 223:186.

11. Bossen, C. et al. (2006) J. Biol. Chem. 281:13964.

12. Xu, Y. et al. (2007) Blood 109:4097.

13. Wang, J. et al. (2005) J. Immunol. 174:8173.

14. Steinberg, M.W. et al. (2008) J. Exp. Med. 205:1463.

• Long Name:

  Herpesvirus Entry Mediator

• Entrez Gene IDs:

  8764 (Human); 230979 (Mouse); 102137807 (Cynomolgus Monkey)

• Alternate Names:

  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