HVEM/TNFRSF14 Antibody (2024B) [Unconjugated]

Mouse splenocytes were stained with Rabbit Anti-Mouse HVEM/TNFRSF14 Monoclonal Antibody (Catalog # MAB2516, filled histogram) or isotype control antibody (Catalog # AB-105-C, open histogram), followed by Phycoerythrin-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # F0110). View our protocol for Staining Membrane-associated Proteins.

CHO Chinese hamster ovary cell line transfected with mouse HVEM was stained with Rabbit Anti-Mouse HVEM/TNFRSF14 Monoclonal Antibody (Catalog # MAB2516, filled histogram) or isotype control antibody (Catalog # AB-105-C, open histogram), followed by Phycoerythrin-conjugated Anti-Rabbit IgG Secondary Antibody (Catalog # F0110). View our protocol for Staining Membrane-associated Proteins.

• Reactivity: Mu
• Applications: Flow
• Clone: 2024B
• Clonality: Monoclonal
• Host: Rabbit
• Conjugate: Unconjugated

HVEM/TNFRSF14 Antibody (2024B) [Unconjugated] Summary

• Additional Information: Recombinant Monoclonal Antibody.
• Immunogen: Chinese hamster ovary cell line CHO-derived recombinant mouse HVEM/TNFRSF14
  Gln39-Val207
  Accession # NP_849262
• Specificity: Detects mouse HVEM/TNFRSF14 in direct ELISAs.
• Source: N/A
• Isotype: IgG
• Clonality: Monoclonal
• Host: Rabbit
• Purity Statement: Protein A or G purified from cell culture supernatant

Applications/Dilutions

• Dilutions:
  • Flow Cytometry 0.25 ug/10^6 cells

Packaging, Storage & Formulations

• Storage: Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
  • 12 months from date of receipt, -20 to -70 °C as supplied.
  • 1 month, 2 to 8 °C under sterile conditions after reconstitution.
  • 6 months, -20 to -70 °C under sterile conditions after reconstitution.
• Buffer: Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. *Small pack size (SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
• Preservative: Sodium Azide
• Reconstitution Instructions: Reconstitute at 0.5 mg/mL in sterile PBS.

Notes

* Contains <0.1% Sodium Azide, which is not hazardous at this concentration according to GHS classifications. Refer to SDS for additional information and handling instructions.

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

Alternate Names for HVEM/TNFRSF14 Antibody (2024B) [Unconjugated]

• 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) 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 (lymphotoxins, exhibits inducible expression, and competes with HSV glycoprotein D for HVEM, a receptor expressed by T lymphocytes) (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).

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.

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.

Bioinformatics

• Uniprot:
  • NP_849262(Mouse)