anti-BTLA (human), mAb (6F4)
|Synonyms||B and T Lymphocyte Associated; Lymphotoxin-β Receptor; Tumor Necrosis Factor Receptor 2 Related Protein; Tumor Necrosis Factor C Receptor; Tumor Necrosis Factor Receptor Superfamily Member 3; TNFRSF3|
|Product Type||Monoclonal Antibody|
|Source/Host||Purified from concentrated hybridoma tissue culture supernatant.|
|Immunogen/Antigen||Ectodomain of human BTLA fused to human IgG Fc.|
Flow Cytometry: Binds to BTLA and to BTLA-HVEM.
Recognizes human BTLA.
|Endotoxin Content||<0.001EU/µg purified protein.|
|Formulation||Liquid. In PBS containing 10% glycerol.|
|Isotype Negative Control|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
After opening, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
|Use/Stability||Stable for at least 1 year after receipt when stored at -20°C.|
|Product Specification Sheet|
B and T lymphocyte associated (BTLA) is an Ig domain superfamily protein with cytoplasmic immunoreceptor tyrosine-based inhibitory motifs. The herpes virus entry mediator (HVEM), a member of the TNF receptor (TNFR) superfamily, can act as a molecular switch that modulates T cell activation by propagating positive signals from the TNF-related ligand LIGHT (TNFR superfamily 14), or inhibitory signals through the Ig superfamily member BTLA. The binding site on HVEM for BTLA is conserved in the orphan TNF receptor UL144, present in human CMV. UL144 binds BTLA, but not LIGHT, and inhibits T cell proliferation, selectively mimicking the inhibitory function of HVEM. BTLA also interacts with HVEM in cis, forming a heterodimeric complex in naive T cells that inhibits HVEM-dependent signaling. The cis-interaction between HVEM and BTLA is the predominant form expressed on the surface of naive human and mouse T cells and may be important to limit trans-signaling by LIGHT, BTLA, and CD160 that are expressed in adjacent activated cells.
- T Cell Intrinsic Heterodimeric Complexes between HVEM and BTLA Determine Receptivity to the Surrounding Microenvironment: T.C. Cheung, et al.; J. Immunol. 183, 7286 (2009)
- Unconventional ligand activation of herpesvirus entry mediator signals cell survival: T.C. Cheung, et al.; PNAS 106, 6244 (2009)