Anti-Mouse TIGIT (1G9) - FITC (T738-GRP)

TIGIT is an immunoreceptor that inhibits multiple immune cell responses, including T cell priming by dendritic cells, tumor cell killing by NK cells and cytotoxic T cells, and also enhances the immune suppressive activity of regulatory T cells1. TIGIT is a novel member of the Ig-superfamily distantly related to Nectins and Necls that aligns with the distal Ig-V-type domains of Nectin1-4, poliovirus receptor (PVR; CD155), DNAM-1 (CD226), and TACTILE (CD96)2. TIGIT is an attractive target for cancer therapy due to its role as an immune checkpoint1,3. Immunotherapy targeting TIGIT and the PD-1/PD-L1 pathway is capable of tumor suppression. 1G9 was generated by immunizing TIGIT-/- mice with recombinant mouse TIGIT tetramers3. Draining lymph nodes were collected and fused with Sp2/0-Ag14. Supernatants were screened for specific binding by anti-TIGIT ELISA and flow cytometry. Hybridomas that showed TIGIT-specific binding were expanded and subcloned and single colonies sorted by flow cytometry. Comparative immunofluorescence staining of activated primary TIGIT-expressing wildtype T cells and TIGIT-/- T cells was performed to confirm specificity. 1G9 was found to fully block TIGIT binding to CD155, a high-affinity TIGIT ligand. However, 1G9 does not deplete TIGIT+ cells in vivo under steady-state conditions. Additionally, 1G9 does not affect T cell proliferation in vitro. 1G9 has agonistic anti-TIGIT activity in vivo, leading to a reduction in T cell expansion and pro-inflammatory cytokine production, and is also able to reduce experimental autoimmune encephalomyelitis (EAE) severity in mice.