BTLA (B and T lymphocyte attenuator) and HVEM (herpesvirus entry mediator) are two important immune regulatory proteins that interact with each other, forming a crucial immune regulatory pathway. BTLA is an inhibitory co-stimulatory receptor that, when bound to HVEM, suppresses T cell activation and immune response. Regulation through the BTLA-HVEM pathway can modulate the activation and function of immune cells, thereby influencing the extent and nature of immune responses.PD-1 (programmed cell death protein 1) is a cell surface receptor mainly expressed on activated T cells, B cells, and NK cells, which can inhibit T cell activation and immune response by binding to its ligands PD-L1 and PD-L2. PD-L1 (programmed cell death ligand 1) is the ligand for PD-1 primarily expressed on tumor cells, immune cells, and tissue cells. Through binding to PD-1, PD-L1 inhibits T cell activation and promotes immune evasion. The PD-1/PD-L1 signaling pathway plays a crucial role in regulating immune tolerance and suppressing autoimmunity by maintaining immune balance through inhibiting T cell activation and inducing T cell exhaustion.The BTLA PD-1 Reporter Cell Line is a gene reporter cell line stably expressing BTLA and PD-1 genes. When co-cultured with the HVEM PD-L1 aAPC CHO-K1 Cell line, binding of BTLA to HVEM and PD-1 to PD-L1 both inhibit T cell signaling. Addition of Anti-BTLA and Anti-PD1 antibodies separately blocks BTLA-HVEM and PD-1-PD-L1 interactions, thereby restoring T cell signaling. This cell line can be used for research on BTLA and PD-1 related drugs.
