CD8 (cluster of differentiation 8)

Its high expression integrates tumor-intrinsic programs (cell cycle, EMT, hypoxia) with tumor-extrinsic immune activation, predicts differential drug sensitivities, and outperforms established biomarkers in forecasting response to immune-checkpoint blockade-particularly in MSI-high disease. These findings nominate IFI30 as a promising diagnostic marker and therapeutic target.

Overall, LILRB1 serves as a key immune checkpoint driving cytotoxic dysfunction, marking exhausted CD8+ T cells and CD16+ NK cells. The nine-gene signature links CD8+ T-cell impairment to poor prognosis, while NK-cell involvement positions LILRB1 as a promising therapeutic target for restoring anti-leukemic immunity.

Ultimately, total activation of CD8+ T cells was decreased in tumor tissues in Tnxb-/- mice. In conclusion, we found that although Tnxb-/- CD4+ and CD8+ T cells tend to be activated more than WT CD4+ and CD8+ T cells, CD8+ T cell infiltration and activation level were attenuated in tumor sites of Tnxb-/- mice.

Immune markers, particularly the CD8/CD4 ratio and CD56-positive lymphocytes, were significantly associated with survival outcomes independent of traditional histopathologic factors. Incorporating immune profiling into risk stratification may improve prognostication and guide the development of immune-targeted strategies in SNMM.

This "pro-tumor vs. anti-tumor" duality underscores the pivotal yet paradoxical role of Type II immunity in tumor immunoregulation. Here, we systematically review the dual functions of Type II immune responses in tumor immunity and their translational potential for next-generation cancer immunotherapy.

The observation group demonstrated superior improvement in Child-Pugh and ALBI scores for patients with mild, moderate, and severe disease after treatment compared to the control group. Conclusion Plasma exchange therapy can effectively improve the immune, liver, and coagulation functions of patients with hyperbilirubinemia of different severity levels following liver cancer surgery, thereby offering significant clinical benefits.

In post-hoc analyses, median progression-free survival was 26 months (95% CI: 14.7-34.3), and median overall survival was 38 months (95% CI: 27.9-not reached). Exploratory gene expression, immunohistochemistry and spatial transcriptomics showed increased intratumoral plasma cells and CD8 T cells in treated patients versus mFFX-only controls, and lymphoid aggregates with high plasma-cell-to-B cell ratios enriched for terminally exhausted CD8 T cells with fewer progenitor exhausted CD8 T cells and central memory CD4 T cells.

Although challenges remain, including delivery specificity, biosafety, biomarker standardization, and off-target effects, the convergence of circRNA biology and advanced nanotechnology presents a transformative opportunity to develop next-generation RNA-guided cancer immunotherapies. Together, these findings position circRNAs as both key mechanistic drivers of immune escape and promising therapeutic targets for nanomedicine-enabled precision immunotherapy.

In bone metastatic mouse models, a combined anti-PD-1/TIGIT immune therapy effectively suppressed tumor cell proliferation and significantly enhanced the cytotoxic activity of CD8+ T cells. Our results provide a systematic view of the molecular basis of BM and suggest future avenues for immunotherapy optimization for BM patients.

Upon ultrasound exposure as an "exogenous switch," activated Ce6, together with Vitamin K3 and Mn2+, induces a robust ROS storm, resulting in mitochondrial dysfunction and immunogenic cell death (ICD), while effectively reprogramming the chronic hypoxia-HIF-2α-driven immunosuppressive tumor microenvironment. Furthermore, in vivo studies demonstrated that Lenvatinib therapy, when combined with the nanoplatform, further suppressed chronic hypoxia-HIF-2α-driven abnormal angiogenesis, enhanced CD8+ T-cell infiltration, and boosted antitumor immune responses, ultimately achieving a potent synergistic therapeutic effect and promoting the conversion of "cold tumors" into "hot tumors." This study provides strong experimental evidence that nanoplatform-mediated immune microenvironment reprogramming represents a precisely controllable and highly effective therapeutic strategy for solid tumors, with promising translational potential in hepatocellular carcinoma.

Complementary transcriptomic analysis using a compact four-gene Tα1 Response Index (Tα1-RI: TLR9, TLR2, IRF1, NLRC5) in TCGA-BRCA (n = 1,112) confirmed positive correlations with antigen presentation and cytotoxic programs and enrichment in CD8-like T cells in single-cell datasets. Collectively, these findings demonstrate that Tα1 enhances CD8+ T cell cytotoxicity while alleviating exhaustion, supporting its potential as an adjunct immunomodulator for improving immune surveillance in breast cancer.

P2, N=35, Recruiting, Sun Yat-sen University Cancer Center; Sun Yat-sen University Cancer Center