Cat. No.
MABL-3479
Application
Blocking, functional assays, IP, WB, FC
Isotype
Engineer antibody
Species Reactivity
Mouse
Clone No.
HMHV-1B18
From
Recombinant Antibody
Specificity
This antibody is specific for Herpes Virus Entry Mediator (HVEM, TR2), a type I transmembrane protein of TNF-receptor superfamily. This receptor, which is expressed on most cell types, including T cells, B cells, monocytes, neutrophils, and dendritic cells. Binding of HSV viral envelope glycoprotein D (gD) to this receptor protein has been shown to be part of the viral entry mechanism. The cytoplasmic region of HVEM was found to bind to several TRAF family members, which may mediate the signal transduction pathways that activate the immune response. HVEM has also been demonstrated to be a unique ligand for BTLA (B and T lymphocyte attenuator). The conservation of the BTLA-HVEM interaction between mouse and human suggests that this system is an important pathway regulating lymphocyte activation and/or homeostasis in the immune response.
Alternative Names
CD270; TNF Receptor-like 2; ATAR; Herpes virus Entry Mediator A; HVEA; Herpes virus Entry Mediator; LIGHTR; Tumor Necrosis Factor Receptor-Like Gene2; Tumor Necrosis Factor Receptor-Like 2; TR2; Tumor Necrosis Factor Receptor Superfamily Member 14; TNFRSF14; CD40-Like Protein
UniProt
Q71F55
Immunogen
This antibody was raised by immunising Armenian hamsters with mouse HVEM: Fc fusion protein.
Application Notes
This antibody has been used in FACS to demonstrate that lymphatic endothelial cells mediate deletion only via programmed cell death-1 (PD-1) ligand 1 (Tewalt et al 2012) and in Western Blot to study the role of LIGHT in the pathogenesis of hepatitis (Anand et al 2006). This antibody has been also been used in vivo experiments to study the mechanisms by which TNFSF14 functions to promote airway remodelling in asthma (Sibilano et al 2016), to confirm that costimulatory role through HVEM is not necessary for LIGHT-mediated liver inflammation (Anand et at 2006), and to investigate the role that herpesvirus entry mediator plays in the development of experimental conjunctivitis (Ishida et al, 2012). Treatment with this antibody has been observed to diminish plasma levels of antigen-specific IgG1 and IgE antibodies in mouse asthma models (Sibilano et al 2016), to interfere with the LIGHT-HVEM interaction but not interaction between B and T lymphocyte attenuator (BTLA) and HVEM in mouse hepatitis models (Anand et at 2006), and NOT to affect the development of experimental conjunctivitis in either the induction or the effector phase (Ishida et al, 2012).
Antibody First Published
Waka Ishida et al. B and T lymphocyte attenuator regulates the development of antigen-induced experimental conjunctivitis. Graefes Arch Clin Exp Ophthalmol. 2012 Feb;250(2): 289-95. PMID: 21779950
Note on publication
Describe the use of this antibody, together with the anti-BTLA antibody, to investigate the roles that B and T lymphocyte attenuator (BTLA) and herpesvirus entry mediator (HVEM) play in the development of antigen-induced experimental conjunctivitis (EC).
Size
100 μg Purified antibody.
Concentration
1 mg/ml.
Purification
Protein A affinity purified
Buffer
PBS with 0.02% Proclin 300.
Storage Recommendation
Store at 4⁰C for up to 3 months. For longer storage, aliquot and store at - 20⁰C.
