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]
|