{"type":"root","children":[{"type":"paragraph","children":[{"type":"text","value":"TIGIT (T cell immunoreceptor with Ig and ITIM domains) is an immune receptor present on some T cells and Natural Killer Cells (NK). It is also identified as WUCAM and Vstm3. TIGIT could bind to CD155 (PVR) on dendritic cells (DCs), macrophages, and other immune cells with high affinity, and also to CD112 (PVRL2) with lower affinity. Research has shown that TIGIT-Fc fusion protein could interact with PVR on dendritic cells and increase its IL-10 secretion level/decrease its IL-12 secretion level under LPS stimulation, and also inhibit T cell activation in vivo. TIGIT"},{"type":"text","value":"'"},{"type":"text","value":"s inhibition of NK cytotoxicity can be blocked by antibodies against its interaction with PVR, and the activity is directed through its ITIM domain."}]},{"type":"paragraph","children":[{"type":"text","value":"TIGIT is expressed on regulatory T cells (Tregs) and on activated CD4+ T, CD8+ T, and NK cells. TIGIT and PD-1 has been shown to be over-expressed on tumor antigen-specific (TA-specific) CD8+ T cells and CD8+ tumor infiltrating lymphocytes (TILs) from individuals with melanoma. Blockade of TIGIT and PD-1 led to increased cell proliferation, cytokine production, and degranulation of TA-specific CD8+ T cells and TIL CD8+ T cells, therefore it can be considered an immune checkpoint. Co-blockade of TIGIT and PD-1 pathways elicits tumor rejection in preclinical murine models."}]}]}