Flow cytometric analysis of Human Peripheral Blood cells labelling Human TIGIT antibody at 1/2000 (0.1 μg) dilution/ (Right panel) compared with a Mouse IgG2a, κ Isotype Control / (left panel). Goat Anti-Mouse IgG Alexa Fluor® 647 was used as the secondary antibody. Then cells were stained with CD3 - Brilliant Violet 421™ antibody separately.
Product Details
Product Details
Product Specification
Host | Mouse |
Antigen | TIGIT |
Synonyms | T-cell immunoreceptor with Ig and ITIM domains; V-set and immunoglobulin domain-containing protein 9; V-set and transmembrane domain-containing protein 3; VSIG9; VSTM3 |
Location | Cell membrane, Synapse |
Accession | Q495A1 |
Clone Number | S-R730 |
Antibody Type | Mouse mAb |
Isotype | IgG2a,k |
Application | FCM |
Reactivity | Hu |
Positive Sample | Human Peripheral Blood |
Purification | Protein A |
Concentration | 2 mg/ml |
Conjugation | Unconjugated |
Physical Appearance | Liquid |
Storage Buffer | PBS pH7.4 |
Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied. |
Dilution
application | dilution | species |
FCM | 1:2000 | Hu |
Background
TIGIT (T cell immunoglobulin and ITIM domain) is an inhibitory receptor expressed on lymphocytes, including natural killer (NK) cells and various subsets of T cells such as CD4+ T cells, CD8+ T cells, and regulatory T cells. It was discovered in 2009 through genome-wide analysis aiming to identify proteins containing domain structures typical for immunomodulatory receptors. TIGIT consists of one extracellular immunoglobulin variable domain, a type I transmembrane domain, and a short intracellular domain with one immunoreceptor tyrosine-based inhibitory motif (ITIM) and one immunoglobulin tyrosine tail (ITT)-like motif. Its main ligand is CD155, also known as poliovirus receptor (PVR), but it can also bind to CD112 and CD113 with lower affinity. TIGIT plays a significant role in down-regulating T cell and NK cell functions by interacting with these ligands expressed on antigen-presenting cells or tumor cells. This interaction inhibits immune cell responses at multiple steps of the cancer-immunity cycle, such as impairing T cell priming by dendritic cells, preventing tumor cell killing by NK cells and cytotoxic T cells, and enhancing the immune suppressive activity of regulatory T cells. Therefore, TIGIT has emerged as a major target in cancer immunotherapy. Several monoclonal antibodies that block the inhibitory activity of human TIGIT have been developed, and clinical trials are ongoing to investigate TIGIT blockade as a monotherapy or in combination with anti-PD1/PD-L1 antibodies for the treatment of patients with advanced solid malignancies.
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