PVR (PVR Cell Adhesion Molecule)

Firstly, we demonstrated that the bispecific antibody (HB0036) for PD-L1 and TIGIT co-blockade induced a greater T-cell proliferative response in vitro compared to the combined administration of the parental antibodies...Lastly, considering the heterogeneity of tumors, we analyzed how the expression patterns of PD-L1 and CD155 influence T cell responses. We also examined the spatial distribution of PD-L1 and CD155, along with related immunological parameters from patient samples, to assess the potential of PD-L1 and TIGIT co-blockade in diverse tumor contexts.

In external transcriptomic validation (TCGA-CRC), GSEA indicated enrichment of interferon/inflammatory programs in TIGIT-high tumors, while CD155-high tumors preferentially showed proliferation-related MYC/E2F/G2M signatures. Together, these findings support tumor-wide upregulation of the TIGIT/CD155 axis in CRC and suggest that TIGIT, more than CD155, tracks with MSI/BRAF-associated immune activation, providing a rationale for patient stratification in checkpoint-directed immunotherapy.

CD155 emerges as a promising therapeutic target for CAR-T therapy in OC. The bispecific CAR-T construct that co-targets CD155 and ROR1 demonstrates superior and durable tumoricidal activity, offering new perspectives on OC targeted therapy.

Finally, DSP502 inhibited tumor growth by potentiating antitumor immunity in xenograft ovarian and lung cancer models. Collectively, these findings demonstrate that DSP502, by blocking PVR and PD-L1 pathways, has dual ICI activity and holds potential therapeutic benefits for cancers such as NSCLC.

Recent advances in NK cell-based immunotherapies-such as cytokine modulation, adoptive NK transfer, and checkpoint blockade-have demonstrated potential to reverse NK exhaustion and enhance antitumor efficacy. In this review, we systematically dissect the molecular and cellular pathways underlying NK cell suppression in ovarian cancer and evaluate emerging strategies to reinvigorate NK-mediated immunosurveillance.

By 48 h, control and R848 nearly closed the wound, unlike the DOX group. R848 and doxorubicin possess anti-proliferative and pro-apoptotic effects on 4T1 cells, doxorubicin effectively induces cell death and boosts immune checkpoint gene expression, while R848 fosters early apoptosis without raising checkpoint ligand expression.

The vaccine promotes T cell infiltration and effector function while upregulating the PVR-TIGIT checkpoint axis. Combining vaccination with TIGIT blockade achieves synergistic anti-tumor efficacy by enhancing antigen-specific CD4 T cell function and delaying exhaustion, providing a promising strategy to overcome immunotherapy resistance in cold tumors.

We identify a novel CD155/YAP/TEAD1/GLUT1 axis that reprograms LUAD metabolism and facilitates immunosuppressive tumor microenvironment formation. CD155 functions as a metabolic-immune hub in LUAD, and its targeting could simultaneously suppress tumor growth and restore antitumor immunity, offering dual therapeutic advantages. Clinically, 18F-FDG PET/CT represents a noninvasive biomarker for CD155-driven metabolic aggression, potentially guiding precision immunotherapy.

HFD-induced metabolic stress drives immune evasion via the STAT3/CD155 axis. Targeting this pathway may improve ICB efficacy in obesity-related cancers.

OPN drives HCC progression by suppressing CD8+ T-cell immunity through the NF-κB (p65)/c-Myc/CD155 axis. Targeting this pathway may enhance anti-tumor immunity and represents a promising therapeutic strategy for HCC.

Overall, our findings provide strong evidence for the efficacy and safety of CD155-based CAR T-cell therapy in cervical and breast cancer. This study contributes to the growing body of research supporting the potential clinical application of CD155-targeted immunotherapy for patients with cervical and breast cancer.

Our findings suggest that TIGIT and CD96 could be markers of the clinical stage and treatment response of HNSCC. Therefore, administering anti-TIGIT and anti-CD96 after radiotherapy may provide a novel approach for incorporating immunoradiotherapy into HNSCC treatment.