CD8 (cluster of differentiation 8)

CST7 contributes to enhanced ICI and boosts the efficacy of PD-1 immunotherapy, suggesting its potential as a therapeutic option for LIHC.

Importantly, CPCs-JPH promotes dendritic cell maturation, activates CD8+ T-cell responses, and significantly improves survival outcomes in orthotopic 4 T1 tumor-bearing mice. This work establishes a multifunctional and enzyme-responsive nanoplatform that harnesses ferroptosis to overcome therapeutic resistance while concurrently engaging innate and adaptive immunity in TNBC.

A transcriptional signature enriched in VISTA-deficient cytotoxic T cells correlated with favorable outcomes in cancer patients treated with existing immune checkpoint inhibitors. These findings collectively define T cell-intrinsic mechanisms by which VISTA enforces T cell dysfunction and underscore its potential as both a therapeutic target and a biomarker of resistance to current immunotherapies.

The control group received DEB-TACE plus the targeted therapy lenvatinib, whereas the observation group was administered DEB-TACE plus lenvatinib and the ICI pembrolizumab. No significant differences were observed in PFS or PFSR between groups(both P > 0.05). The combined use of DEB-TACE, targeted therapy and an ICI demonstrates superior clinical efficacy and a favorable safety profile, which can reduce tumor marker levels, enhance immune function and prolong OS in patients with intermediate-to-advanced HCC.

This study highlights the therapeutic efficacy of α2-AR agonists in osteosarcoma treatment through a novel drug delivery system, suggesting their potential to enhance anti-tumor immune responses by modulating CD8+ T cell activity and TCR signaling, as supported by correlations with clinical outcomes in TCGA and GTEx databases. The findings of this study present a promising translational potential by demonstrating the efficacy of α2-AR agonists in enhancing anti-tumor immunity in OS, potentially paving the way for targeted immunotherapies in post-surgical management to combat tumor recurrence and resistance.

This study highlights the importance of spatial niches in understanding the TIME of NSCLC and predicting ICB responses. CYP27A1+TAMs and their downstream LXR pathway provide a novel research direction for exploring potential biomarkers for personalized NSCLC management.

Although cross-presentation is still inhibited in the presence of a high BCG MOI (0.4), it rebounds by reducing tenfold the BCG MOI from 0.4 to 0.04. This suggests that an adequate balance between tumor antigens and BCG phagocytosis is needed to retain the stimulatory properties of activated monocytes and trigger immunogenicity of tumor antigens.

Specifically, it elucidates how ferroptosis modulates immune cells such as CD8+ T cells and macrophages, reshaping the tumor immune microenvironment and offering new avenues for combination immunotherapy. We conclude by providing a roadmap for translating these insights into clinical practice, addressing current challenges, and outlining future directions for developing next-generation anticancer strategies.

Our findings propose a model wherein an imbalance in CD8+ T cell differentiation, favoring aggressive cytotoxic effectors over a putative buffering transitional population, underpins irAEs pathogenesis in acral melanoma patients receiving anti-PD-1 therapy. The transitional-to-cytotoxic CD8+ T cell ratio emerges as an exploratory candidate biomarker for irAEs risk, warranting validation in larger prospective cohorts.

Co-culture experiments showed that ALKBH5 knockdown enhanced the proportion of CD8+ T cells and secretion of IFN-γ/TNF-α, and reduced the survival rate of AML cells. ALKBH5 may promote AML progression and immune escape through the upregulation of PD-L1 and modulation of T-cell function, which provides a theoretical basis for the development and screening of novel immunotherapeutic strategies for AML.

Our findings suggest that intratumoral CD8+ TILs are an independent predictor of the efficacy of neoadjuvant therapy in breast cancer. In the future, incorporating intratumoral CD8+ TILs into existing clinicopathological predictive models and combining their assessment with other immune biomarkers may enable the development of more robust predictive tools, thereby providing a solid foundation for truly individualized and precision-based neoadjuvant treatment in breast cancer.

NG25 blocks the NF-κB signaling pathway by targeting TAK1, remodels the immunosuppressive microenvironment of KRAS-mutated colorectal cancer, reduces PD-1 expression and enhances the anti-tumor effect of CD8⁺ T cells. This study provides a theoretical basis for TAK1-targeted therapy and offers a new strategy for immunotherapy of KRAS-mutated colorectal cancer.