GZMB (Granzyme B)

Collectively, these findings indicate that CEP55 promotes liver cancer immune escape and malignant progression through modulation of STAT1-dependent PD-L1/MHC-I expression, oxidative stress, and immunosuppressive signaling. Targeting CEP55 may therefore represent a potential strategy to improve antitumor immune recognition in liver cancer.

(-)-Gallocatechin gallate and indomethacin bound well to GZMB, while benzo(a)pyrene and benzo(e)pyrene had good binding potential with LSP1. We established lactylation as a critical regulator of AML, and GZMB and LSP1 were identified as lactylation-related clinical modeling indicators, which provides a foundation for choosing prognostic and therapeutic strategies for AML.

CD86high CD8+ T cells constitute a distinct immunoregulatory subset in cancer. Their differentiation is driven by an IL-12-IRF5 program, and their crosstalk with DCs via CD86/CTLA-4 engagement promotes tolerogenic remodeling of the TME. Targeting CD86 on CD8+ T cells may disrupt this suppressive circuit and potentiate antitumor immunity.

Mechanistically, UA was associated with modulation of the AKT/mTOR signaling pathway to limit tumor progression and with alterations in AKT1-related signaling, including changes in the P-AKT1/FOXO1 axis and increased expression of cytotoxic effector molecules such as GZMB, thereby contributing to antitumor immune activation and remodeling of the tumor immune microenvironment. This study proposes a working model of a diet-microbiota-AKT1-immunity axis, which may provide conceptual insights into CRC prevention and immunotherapeutic strategies.

Older tissues had a more inflammatory microenvironment with increased M2 macrophages and granzyme B+ T cells, contrasted by younger tissues in which B cells were most enriched. Our multiscale atlas extensively details an unexpected general decline of breast tissue with age and reveals its changing spatial context.

SCFAs and IN exert modest but selective effects on apoptosis and inflammatory pathways in HNSCC, whereas cytotoxic activity remains stable. These results support the potential of tailoring metabolic and nutritional interventions to individual patients to modulate the tumor immune microenvironment, and provide a rationale for integrating SCFAs and IN with immunotherapeutic strategies in HNSCC.

These findings reveal a previously unrecognized, cell-extrinsic role for Irgm1 in regulating CD8+ T cell survival and function by modulating the inflammatory environment. Our results suggest that IRGM/Irgm1 acts as a critical immune rheostat, restraining pathological inflammation and modulating T cell responses in infection and autoimmunity.

This study demonstrates that HQ potentiates NK cell anti-tumor immunity against prostate cancer through a dual mechanism involving PI3K/AKT pathway activation and PD-1/PD-L1 axis inhibition. These findings provide modern pharmacological evidence supporting the traditional use of HQ for enhancing immune surveillance in cancer therapy.

FLT3-IL2-CAR-γδT cells considerably slowed the development of AML in vivo and extended the existence (>68 days) of mice. FLT3-IL2-CAR-γδT cells exhibit potent and durable anti-AML activity, providing a novel strategy for clinical AML immunotherapy.

In turn, these microbes produced beneficial metabolites such as SCFAs, particularly butyric acid, which likely contributed to the antitumor effects. Overall, Post18 supplementation represents a potential strategy for alleviating HCC and provides a foundation for developing additional treatment options.

Our study provides further insight into the composition of the gut microbiota in dogs with MCTs, where ECT and IL-12 GET did not lead to major shifts. We were unable to establish any association between the expression of immune markers and the microbiota.

E3C4 constitutes a localized, synergistic platform that enables dual-antigen T cell co-activation within the peritoneal cavity. This approach maximizes antitumor efficacy while circumventing systemic toxicity, offering a novel immunotherapeutic strategy for GCPM.