PD1/TIGIT Dual Effector Reporter Cell
The binding of Programmed Cell Death Protein 1 (PD-1), a receptor expressed on activated T-cells, to its ligands, PD-L1 and PD-L2, negatively regulates immune responses. PD-1 ligands are found on most cancers, and the PD-1:PD-L1/2 interaction inhibits T-cell activity and enables cancer cells to escape immune surveillance. The PD-1:PD-L1/2 pathway is also involved in regulating autoimmune responses, making these proteins promising therapeutic targets for a number of cancers, as well as multiple sclerosis, arthritis, lupus, and type I diabetes.
TIGIT is a co-inhibitory receptor that is highly expressed in Natural Killer (NK) cells, activated CD4+, CD8+ and regulatory T cells. Interaction with the poliovirus receptor (PVR; CD155) on antigen presenting cells, such as dendritic cells, recruits Src homology (SH) domain-containing protein tyrosine phosphatase SHP1 and SHP2 or the inositol phosphatase SHIP1 and SHIP2 to the TIGIT ITIM domain. This increases IL-10 release and suppresses NF-kB and NFAT T cell receptor (TCR) signaling, which blocks T cell proliferation and cytokine production. It serves as a competitive inhibitor of CD226, a co-stimulatory receptor for CD155. TIGIT targeting antibodies that block this T cell-intrinsic inhibitory effects have shown enhanced anti-tumor and anti-viral functions in preclinical studies.
|Stability:||32 passages (in-house test, that not means the cell line will be instable beyond the passages we tested.)|
|Freeze Medium:||90% FBS+10% DMSO|
|Culture Medium:||F12K+10%FBS+600ug/ml hygromycin+2ug/ml puromycin+5ug/ml blasticidin|
|Application(s):||Functional(Report Gene) Assay|
|III. Representative Data|
Figure 1. Dose Response of Blocking Antibodies in PD-1/TIGIT Dual Effector Reporter Cells (Clone 7) With PD-L1&CD155/ TCR Activator - CHO Cells.
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