NECTIN2 (Nectin Cell Adhesion Molecule 2)

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.

These findings provide mechanistic insights into immune evasion and suggest NECTIN-TIGIT signaling as a potential biomarker and therapeutic target. Future wet-laboratory validation and clinical studies are needed to confirm the translational relevance of this axis in thyroid cancer management.

Through systematic analysis, we developed a 12 PR-mRNAs signature that effectively predicts clinical outcomes in TNBC patients. The newly established risk assessment model not only provides a reliable tool for prognostic evaluation but also reveals NECTIN2 as a clinically significant biomarker, with elevated expression correlating with poorer survival outcomes.

Similarly, NK cell recognition of targets expressing the nectin CD112, which also engages both DNAM-1 and TIGIT, resulted in modest loss of DNAM-1 expression and heightened IFN-γ responses. Together, these observations suggest that DNAM-1 recognition of its ligands is delicately poised such that low avidity receptor engagement augments NK cell activation, and in particular IFN-γ responses, while stronger engagement can result in the rapid downregulation of DNAM-1 without any significant enhancement of effector responses.

Our findings suggest that targeting the SPP1-CD44, NECTIN2-TIGIT, and HLA-E-CD8B pathways may improve immune responses in NSCLC. These findings provide novel therapeutic targets and highlight the potential for combination immunotherapies to overcome macrophage-mediated immune evasion.

This study elucidates the synergistic mechanisms and identifies key resistance pathways underlying chemo-immunotherapy combinations in patients with ESCC, providing a scientific basis for refining future combination therapeutic regimens.

In conclusion, this study demonstrates the dual oncolytic and immunogenic potential of an FLT3L-encoding OV, particularly on cDCs. These findings support the further development of this approach as a novel cancer immunotherapy.

This study represents a significant advancement in the understanding of TR TIL biology and provides a rapid and accurate method to identify TR CD8 TILs.

Retrospective analyses confirmed therapeutic benefit in patients with diabetic PDAC receiving rosuvastatin. These findings uncover a lactate-METTL16-CTCF axis that links metabolic stress to epitranscriptomic reprogramming and immune evasion, offering a promising strategy to potentiate immunotherapy in metabolically dysregulated PDAC.

Growing evidence highlight CD226's emerging promise as a therapeutic target for immune-mediated diseases. The present work aims to review the current understanding of CD226's role in immune responses and to comprehensively outline its multifaceted involvement in different immunological diseases, providing insights for future research to advance our mechanistic understanding of its roles in disease pathogenesis.

This transition from membranous to cytoplasmic localization was also evident in the progression from normal superficial epithelium to malignant tissue. These observations suggest that alterations in the expression and subcellular localization of Nectin-4 may be associated with carcinogenesis and could serve as potential markers for the assessment of precancerous lesions and the aggressiveness of laryngeal tumors.

Furthermore, CLU+_ECs induce CD8+ T cell exhaustion via the Nectin2-TIGIT pathway, suppressing the anti-tumor immune response. Overall, our study highlights the substantial spatial heterogeneity in osteosarcoma and identifies CLU+_ECs in the peripheral region as promising therapeutic targets.