T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domains (TIGIT)

TIGIT is a transmembrane glycoprotein receptor expressed on T cells (especially activated and memory subsets), natural killer (NK) cells, and regulatory T cells (Tregs)[3][4]. It contains a single extracellular immunoglobulin variable domain and a cytoplasmic tail with an immunoreceptor tyrosine-based inhibitory motif (ITIM)[4]. TIGIT binds primarily to CD155 (PVR) as well as CD112 and CD113, transmitting inhibitory signals that dampen T cell and NK cell activation, reduce inflammatory cytokine production, and modulate antigen-presenting cell (APC) function. Expression of TIGIT is upregulated in chronic antigen exposure settings, including cancer and infection, and is associated with immune exhaustion. Therapeutic blockade of TIGIT (often in combination with PD-1/PD-L1 inhibitors) is in clinical development for the treatment of various cancers, aiming to restore anti-tumor immune responses and improve patient outcomes[3][4].

Other names

TIGITT-cell immunoglobulin and ITIM domainVSTM3

Blocking TIGIT prevents its inhibitory signal, allowing T cell and NK cell activation and enhanced anti-tumor immunity Monoclonal antibodies bind to TIGIT, blocking its interaction with ligands (CD155, CD112, CD113) Disrupting TIGIT/CD155 interaction, increasing cytokine secretion and proliferation of effector cells[3][4]