CD226 (CD226 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.

Mechanisms by which KIR3DL1/Bw4 interaction interferes with BCG-induced NK cell proliferation and the production of cytokines and icNO, warrant further investigation. HLA-I genotyping should be investigated as a useful biomarker to personalize BCG immunotherapy in BC.

The CD155-CD226/TIGIT/CD96 immune checkpoint complex expressed on both TME TC and TILs, and interacted with TILs to exhibit diverse prognosis effect on BC. The immunotherapy against these checkpoint proteins should check the expression on both TC and TILs and further studies should explore the molecule complex collectively for comprehensive prediction of BC prognosis.

However, a specific combination of tumoral cells expression of CD226(≥4%), CD155(≥40%), and CD96(≥35%), coupled with TIGIT expression on tumoral (<35%) and stromal cells (<12.5%), was able to identify patients with G1 response to NAC.ConclusionExpression levels of TIGIT/CD155/CD226/CD96 on tumoral and stromal cells might collectively serve as predictive biomarkers for NAC response in TNBC. This implied that CD155-TIGIT axis could be prospectively applied clinically to identify NAC-resistant TNBC patients.

In vivo, treatment with chi2B5×4F11 reduced the proportion of TIGIT+ circulating immune subsets within the CD226+ compartment, suggesting functional restoration of co-stimulatory signaling. These findings highlight TIGIT as a crucial therapeutic target and suggest a strategy to overcome the immune resistance of pancreatic cancer.

This study established a novel prognostic tool for BC by combining TME markers with clinicopathological factors. The developed nomograms enabled accurate individualized risk stratification and demonstrated clinical utility, offering a framework for precision oncology to survival prediction.

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.

Together, these findings highlight that simultaneous modulation of PD-L1 and CD226 pathways can restore CMV-specific T cell function, offering a promising strategy to boost TCR-T efficacy in cytokine-deprived environments. &lsqb;BMB Reports 2025; 58(7): 307-312].

In an AML xenograft model, mice treated with CD226 overexpression iPSC-NK cells exhibited significantly reduced leukemia burden, prolonged survival, decreased systemic inflammation compared to those treated with Control iPSC-NK cells. Overall, our study provided evidence that iPSC derived-NK cells engineered with CD226 represent a promising candidate for off-the-shelf immunotherapy, particularly in AML and other CD226 ligand-expressing malignancies.

Dysregulated expression of TIGIT and its family molecules on NK cells contributes to NK cell dysfunction and promotes tumor immune escape in DLBCL. These findings highlight TIGIT as a promising therapeutic target for restoring NK cell-mediated antitumor immunity in DLBCL.

This suggests parallel but potentially cooperative roles for LFA-1 and CAR38 in synapse formation. Our findings suggest that CAR38 NK cells could be an effective therapeutic strategy to overcome CD226-mediated immune evasion in AML.

Our findings highlight the critical role of CD8+CD226+RUNX2hi T cells in CLL and suggest that their reduction is associated with disease progression and poor clinical outcomes. This study also underscores the potential of targeting IL-6 and MIP-1β to preserve polyfunctional CD8+CD226+ T cells as a promising immunotherapy strategy.