背景介绍 HVEM is a member of the TNFR superfamily that is expressed on T cells, B cells, NK cells and antigen-presenting cells. HVEM is a bidirectional switch that regulates T-cell activation in either a costimulatory or coinhibitory fashion, depending on the binding partner. HVEM can act as both ligand and receptor; the binding of HVEM to BTLA (IgSF) or CD160 on Effector T cells delivers a coinhibitory signal; alternately, the binding of HVEM to either of two tumor necrosis factor ligands, LIGHT or lymphotoxin-α, delivers a costimulatory signal. The HVEM/BTLA axis are co-inhibitory immune checkpoint molecules that play important roles in the blockade of T cell-mediated immune responses. The binding of BTLA, a receptor expressed on activated T-cells, to its ligand HVEM, found on melanoma and other cancers, negatively regulates T cell immune responses and allows cancer cells to escape immune surveillance. This co-inhibitory signal of the HVEM/BTLA interaction can be reversed by treatment with a BTLA blocking antibody. The HVEM/BTLA/LIGHT pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of diseases. 产品介绍 Recombinant CHO-K1 cells constitutively expressing human HVEM (Herpes Virus Entry Mediator), also known as CD270 or TNFRSF14 (Tumor Necrosis Factor Receptor Superfamily Member 14), GenBank Accession No. NM_003820, and an engineered T cell receptor (TCR) activator.