CD155 (Poliovirus receptor) and CD112 (Nectin-2) (CD155 and CD112)

CD155 (Poliovirus receptor) is a single-pass immunoglobulin-like adhesion molecule present on the surface of several cell types, especially epithelial and immune cells. It modulates natural killer (NK) and T cell-mediated immunity by interacting with immune receptors including TIGIT (inhibitory), CD96 (inhibitory), and DNAM-1/CD226 (activating), contributing to immune response regulation, cell adhesion, migration, and tumor cell immune evasion. CD155 is upregulated on tumor cells and recognized as a therapeutic target in cancer immunotherapy, acting as a ligand for both activating and inhibitory immune cell receptors. It is also the host cell receptor for poliovirus entry. CD112 (Nectin-2) is a member of the nectin family of cell adhesion molecules, predominantly found in epithelial junctions but also expressed by other cell types. It acts as a ligand for receptors on immune cells, such as TIGIT (inhibitory) and CD112R (inhibitory), and DNAM-1/CD226 (activating), regulating T cell proliferation, tumor cell adhesion, metastasis, and immune surveillance. Increased CD112 correlates with poor prognosis in some cancers. Blockade of CD112-inhibitory pathways is a strategy in cancer immunotherapy, often in combination with other checkpoint inhibitors. Both molecules play critical roles as immune checkpoint ligands and therapeutic targets, primarily in cancer but also in infection and tissue remodeling contexts. Their main biological functions involve modulation of immune response, cell adhesion, and metastasis.

Other names

PVRNecl-5PVRαPVRδPVRL2Nectin-2Nectin-2αNectin-2δ

Blockade of CD155/TIGIT or CD112/TIGIT pathway to unleash immune cell cytotoxicity against tumors by preventing inhibitory signals mediated by TIGIT and/or CD112R binding. Activation of DNAM-1 pathway to enhance immune cell-mediated tumor cell killing.