CD8 (cluster of differentiation 8)

Targeting surface ENO1 with HuL001, a first-in-class humanized antibody, significantly reduced glycolysis, decreased extracellular lactate accumulation, reprogrammed macrophage polarization and inhibited tumor growth and distant metastasis. Moreover, targeting surface ENO1 significantly increased the therapeutic response to radiotherapy and delayed tumor regrowth by increasing antitumoral M1 macrophages and cytotoxic CD8+ T cells infiltration within TME. These results indicated that targeting surface ENO1 remodeled the tumor microenvironment and provided better therapeutic effects to radiotherapy in poorly immunogenic colorectal cancer (CRC) and triple-negative breast cancer (TNBC).

The obtained results confirm an increased immunoactivation profile in children with VLS, characterized by elevated checkpoint expression and increased levels of proinflammatory cytokines. The studied parameters show potential as diagnostic and prognostic biomarkers, which may constitute the basis for the development of new diagnostic tools and targeted therapeutic strategies in VLS in pediatric patients.

These results indicate that PI3Kγ contributes to cSCC development not by directly driving tumour cell proliferation but by shaping an immunosuppressive tumour microenvironment. Targeting PI3Kγ may therefore represent a promising immunotherapeutic strategy to enhance cytotoxic T-cell-mediated antitumour immunity in cSCC.

Our findings highlight the potential of epigenetic modulators to re-shape the tumor microenvironment of PROC toward a more inflammed phenotype and may point to approaches to augment immunotherapy response.

Treatment-induced EMT reduces GATA6+ populations and MHCI expression, which is restored by combining MEKi with HDAC inhibitors, enhancing GATA6+ tumor cells, MHCI, CD8+ T cell infiltration, tumor suppression, and survival. These findings suggest that therapeutic strategies promoting a GATA6-driven tumor cell state improve immune recognition of PDAC cells and potentiate anti-tumor cytotoxic effects.

CD8+ T cell depletion completely abrogates the anti-tumor effects, suggesting their essential role in mediating therapeutic responses. These findings establish Gal-9 upregulation as a critical adaptive immune resistance mechanism constraining ATRi efficacy, providing a compelling rationale for clinical translation of ceralasertib/Gal-9 blockade combinations.

Moreover, in vivo targets of YAP1 stratify survival in male but not female patients with medulloblastoma, glioblastoma, mesothelioma, and lung cancer. This study provides evidence for sex-biased functions of Yap1 and CD276 in MB immune suppression and highlights the importance of biological sex in cancer:immune interactions.

ETP-ALL represents a biologically distinct T-ALL subtype with inferior early treatment responses. The TCCSG six-marker scoring system is reliable, accurate, and practical for routine diagnosis, particularly in resource-limited settings.

The combination of PARP inhibitors and platinum activates the cGAS-STING pathway, leading to increased infiltration of mature DCs and CD8+ T cells, thereby sensitizing NSCLC to anti-PD-L1 therapy. This study presents a promising strategy for treating patients with LUAD with low immunogenicity and poor prognosis.

In vivo antitumor studies confirmed that the administration of PPS-ICG@PLGA NPs increased the ratio of CD4+ and CD8+ T cells in both tumor and spleen, enhanced DCs maturation in tumor and reversed the intratumor infiltration of regulatory T cells (Tregs) in tumor. These results demonstrate the application potential of PPS in promoting the immunotherapy efficacy of phototherapy, and also propose PPS-ICG@PLGA as a promising nanosystem for photoimmunotherapy.

In contrast, ibrutinib added 48 h post-activation did not show these effects. These findings suggest that caution should be exercised when incorporating ibrutinib into ex vivo expansion system for adoptive non-genetically engineered T cells or combining ibrutinib with these T cell immunotherapies in clinical trial settings.

XYS prevents psychiatric disorder-associated CRC metastasis and strengthens antitumor immune responses by regulating bsh-expressing gut bacteria and their derived BA profiles. These findings thus offer a novel mechanistic rationale for the potential use of XYS in treating CRC patients with comorbid psychiatric disorders.