Cat. No：GM-C07928
Product：H_PD-1 Reporter Jurkat Cell Line
Cat. No：GM-C07928
Product：H_PD-1 Reporter Jurkat Cell Line
Cell Growth Medium：1640+10% FBS+0.75ug/ml Puromycin+3.5ug/ml Blasticidin+1% P.S
Cell Freezing Medium：FBS+10% DMSO
Assay Buffer：1640+1% FBS
PD-1 is an immune-inhibitory receptor expressed on activated T and B cells, playing a crucial role in regulating immune responses to tumor antigens and self-antigens. The interaction of PD-1 on adjacent cells with its ligands PD-L1 or PD-L2 inhibits the transmission of TCR signaling pathways, as well as TCR-mediated cell proliferation, transcription activation, and cytokine production. Therapeutic antibodies and Fc fusion proteins that block the PD-1/PD-L1 interaction have shown promising prospects in clinical trials for treating various cancers. Current methods for measuring the activity of anti-PD-1 or anti-PD-L1 biotherapeutics rely on primary human T cells and functional endpoints such as cell proliferation, cell surface marker expression, interferon-gamma (IFNγ), and interleukin-2 (IL-2) production. These assays are challenging to establish in a quality-controlled drug development environment due to their dependence on donor primary cells, complex experimental protocols, and inadequate assay reagents.
Genomeditech H_PD-1 Reporter Jurkat Cell Line is a reporter gene cell line that stably expresses the H_PD-1 gene and Luciferase reporter gene. When co-cultured with the corresponding aAPC(OKT3) PDL1 CHO-K1 Cell Line (Genomeditech/GM-C05269), which stably expresses human PD-L1 and a cell surface protein that activates homologous TCR in an antigen-independent manner, the interaction between PD-1 and PD-L1 inhibits TCR signaling transduction and transcription factor-mediated luciferase expression. Upon adding antibodies blocking PD-1/PD-L1, this inhibition is relieved, leading to the expression of luciferase mediated by the TCR signaling transduction and transcription factor, useful for assessing the efficacy and stability of antibodies and other biotherapeutics blocking the PD-1/PD-L1 interaction.
Cat. No：GM-C07928
Product：H_PD-1 Reporter Jurkat Cell Line
Cell Growth Medium：1640+10% FBS+0.75ug/ml Puromycin+3.5ug/ml Blasticidin+1% P.S
Cell Freezing Medium：FBS+10% DMSO
Assay Buffer：1640+1% FBS
PD-1 is an immune-inhibitory receptor expressed on activated T and B cells, playing a crucial role in regulating immune responses to tumor antigens and self-antigens. The interaction of PD-1 on adjacent cells with its ligands PD-L1 or PD-L2 inhibits the transmission of TCR signaling pathways, as well as TCR-mediated cell proliferation, transcription activation, and cytokine production. Therapeutic antibodies and Fc fusion proteins that block the PD-1/PD-L1 interaction have shown promising prospects in clinical trials for treating various cancers. Current methods for measuring the activity of anti-PD-1 or anti-PD-L1 biotherapeutics rely on primary human T cells and functional endpoints such as cell proliferation, cell surface marker expression, interferon-gamma (IFNγ), and interleukin-2 (IL-2) production. These assays are challenging to establish in a quality-controlled drug development environment due to their dependence on donor primary cells, complex experimental protocols, and inadequate assay reagents.
Genomeditech H_PD-1 Reporter Jurkat Cell Line is a reporter gene cell line that stably expresses the H_PD-1 gene and Luciferase reporter gene. When co-cultured with the corresponding aAPC(OKT3) PDL1 CHO-K1 Cell Line (Genomeditech/GM-C05269), which stably expresses human PD-L1 and a cell surface protein that activates homologous TCR in an antigen-independent manner, the interaction between PD-1 and PD-L1 inhibits TCR signaling transduction and transcription factor-mediated luciferase expression. Upon adding antibodies blocking PD-1/PD-L1, this inhibition is relieved, leading to the expression of luciferase mediated by the TCR signaling transduction and transcription factor, useful for assessing the efficacy and stability of antibodies and other biotherapeutics blocking the PD-1/PD-L1 interaction.
