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Table 1 Preclinical trials in promising cancer target of PVR like receptors

From: Poliovirus receptor (PVR)-like protein cosignaling network: new opportunities for cancer immunotherapy

PVR like protein Treatment Immune cells Tumor Results Reference
DNAM-1 Anti-DMAN-1 or anti-PVR mAbs NK Neuroblastoma monoclonal antibody-mediated masking of either DNAM-1 (on NK cells) or PVR (on neuroblasts) resulted in strong inhibition of tumor cell lysis [26]
DNAM-1 Anti-DMAN-1 or anti-PVR mAbs NK Tumor cell lines The ability of NK-mediated lysis of tumor cells mediated by DNAM-1 engage with its ligands that was downregulated by mAb-mediated masking of the receptor or its ligands [15]
DNAM-1 anti-CD226 mAb LeoA1 NK Hepatoma Crosslinking CD226 with the anti-CD226 mAb LeoA1 regulate miR-30c-1* expression, which promoted NK cell cytotoxicity against hepatoma cells by targeting HMBOX1 [27]
DNAM-1 DNAM-1 agonist NK Melanoma, experimental autoimmune encephalomyelitis DNAM-1 agonist could activate DNAM-1 modifies the bidirectional crosstalk of NK cells with CD155 DC, which can suppress CNS autoimmunity and strengthen tumor surveillance [28]
DNAM-1 Anti-CD226 mAb Tregs Allogeneic skin transplant CD226 mAb promoted Treg expansion, reduced inflammation and prolonged allogeneic graft survival [29]
DNAM-1 Anti-CD226 mAb γδT Hepatocellular carcinoma Anti-DNAM-1 mAb-mediated masking experiments that γδT cells cytotoxicity against HCC cells as well as IFN-γ production were decreased [30]
DNAM-1 CD226 agonist antibody CD8+ T pancreatic ductal adenocarcinoma CD226 agonist antibody-mediated activation of CD226 augments the effect of TIGIT or PD-1 blockade on CD8 T-cell responses [31]
TIGIT Anti-TIGIT NK Colon cancer Blockade of TIGIT prevented NK cell exhaustion and promoted NK cell–dependent tumor immunity, enhanced therapy with antibody to the PD-1 ligand PD-L1 [32]
TIGIT Anti-TIGIT NK Ovarian cancer Blockade of TIGIT enhanced degranulation and interferon gamma (IFN-γ) production of NK cells in response to OC tumor cells [33]
TIGIT Anti-TIGIT CD8+ T Melanoma TIGIT and PD-1 blockade should be further explored to elicit potent antitumor CD8+ T cell responses [34]
TIGIT Anti-TIGIT CD8+ T Gastric cancer Blockade TIGIT enhanced CD8 T cell activation and improved survival in tumor bearing mice [35]
TIGIT Anti-TIGIT CD8+ T Multiple myeloma Blockade TIGIT by mAb increased the effector function of MM patient CD8+ T cells and suppressed MM development [36]
TIGIT Anti-TIGIT CD8+ T Myeloma Immune checkpoint blockade using mAb against TIGIT significantly restored CD8+ T exhaustion and prolonged myeloma control after stem cell transplantation [37]
TIGIT Anti-TIGIT CD8+ T, Tregs Head and neck squamous cell carcinoma Anti-TIGIT treatment significantly reverse T-cell exhaustion and reduce the population of Tregs in vitro and in vivo [38]
TIGIT Anti-TIGIT CD4+ T, CD8+ T, Tregs Multiple myeloma Anti-TIGIT mAb depleted FoxP3+ Tregs, increased proliferation of IFN-γ-producing CD4+ T cells, and overcame the inhibition effect of CD8+ T cell signaling and cell proliferation by PVR ligation [39]
TIGIT Anti-TIGIT αβT, γδT, Tregs Hematologic malignancies Anti-TIGIT mAbs could restore αβT-cell function, prevent CD155 mediated inhibition of γδ T cells, depletion of Tregs, and direct killing of tumor cells [40]
TIGIT Anti-TIGIT Effector T, Tregs Glioblastoma TIGIT a checkpoint blockade increased effector T cell function and downregulation of suppressive Tregs and TIDCs to enhance antitumor immunity and survival in glioblastoma [41]
TIGIT Anti-TIGIT CD4+ Tregs Ovarian cancer Anti-TIGIT treatment reduced the proportion of CD4+ Tregs [42]
CD96 Anti-CD96 NK Melanoma lung metastases Anti-CD96 enhances the NK cell IFN-γ-dependent effector function, which significantly reduced experimental and spontaneous lung metastases [43]
CD96 Anti-CD96 NK Hepatocellular carcinoma Anti-CD96 antibody of blocking CD96 and its ligand CD155 interaction, the human NK cell lines cytotoxicity was restored and enhanced [44]
CD96 Anti-CD96 NK Tumor metastases CD96 targeted antibodies promote NK cell anti-tumor activity [45]
CD96 Anti-CD96 CD8+ T Anti-tumor Ab blockade on CD8+ T cells could eliminate IFN-γ and/or TNF-α production, which associated with CD8+ T cell activation [46]
CD96 Anti-CD96 CD8+ T Melanoma Anti-CD96 therapy is effective to enhance CD8+ T activity and limit tumor growth [47]
CD96 Anti-CD96 Th19 Inflammatory diseases Blockade of CD96 significantly restored the expansion and inflammatory properties of CD96high Th9 cells [48]
CD112R Anti-CD112R NK Breast cancer Blockage CD112R could improve trastuzumab therapy for breast cancer by enhancing NK cells activity [49]
CD112R Anti-CD112R CD8+ T Melanoma, pancreatic cancer Blockade of PVRIG increased CD8+ T-cell function, an effect enhanced by combination with TIGIT or PD-1 blockade [50]
  1. mAb monoclonal antibody, CNS central nervous system, HCC hepatocellular carcinoma, PD-1 programmed cell death 1, PD-L1 programmed cell death-ligand 1, TIDCs tumor-infiltrating dendritic cells