IFNGR1 (Interferon Gamma Receptor 1)

These findings provide a detailed mutational map of antigen presentation and IFNγ-response components in cancer. Overall, our results provide a resource of specific mutations in genes involved in immune pathways that compromise tumor immunogenicity and will serve for support in patient selection for response to ICB.

PK-H exerts anti-inflammatory effects predominantly through selective inhibition of the JAK-STAT1 pathway. Its diterpenoid constituents represent promising leads for STAT1-targeted anti-inflammatory agents.

The current study shows that the AA genotype of the IFN-γ and TC genotype of the IFN-γR1 genes are associated with increased susceptibility and HCV chronicity. While the TT genotype of the IFN-γ and the CC genotype of the IFN-γR1 may confer a protective effect.

Compared with standard chemoimmunotherapy, PD-L1 blockade combined with BTZ had greater antitumor effects because of the inability of cisplatin (CDDP) and pemetrexed (PEM) to regulate IFNGR1 expression. Notably, compared with BTZ treatment alone, anti-PD-L1 therapy increased BTZ tumor accumulation by promoting microvascular maturation, potentially addressing a major obstacle to the use of BTZ in solid tumors. Taken together, these results suggest that BTZ, when combined with immunotherapy, holds great promise for treating lung cancer.

These data demonstrate that CD8+ T cells contribute to tumor control even in the absence of direct antigen presentation by tumor cells. More broadly, our work suggests that strategies to activate the effector functions of inflammatory monocytes may limit tumor growth and overcome acquired resistance to immune checkpoint inhibitors.

Immunohistochemical analysis revealed higher expression levels of genes HSP90AA1, HMGB1, IFNGR1, PDIA3 in STAD tumor tissues compared to normal tissues. This research developed a prognostic model for STAD using ICDRGs and investigated the potential influence of these genes in patients with GC, providing a new direction for evaluating GC prognosis and guiding individualized treatment.

Lymphatic-specific inhibition of mitochondrial complex III restrained the intratumoral tip-like state, blocked metastasis, and enhanced the response to ICB. Our data reveal that IFNγ induces a metabolic and phenotypic switch in tumor-associated lymphatic vessels that blocks regional metastasis and reinforces immune surveillance.

TMEM199/CCDC115 also recruits transport protein particle (TRAPP) Ⅱ to the recycling endosomes and activates RAB11A, leading to enhanced IFNGR1/2 recycling and downstream PD-L1 upregulation. Collectively, these findings reveal that TMEM199 might be a promising therapeutic target for immunotherapy.

This review aims to provide a comprehensive understanding of OPTN's pleiotropic functions, highlighting its role in autophagy, inflammation, immune surveillance, and cancer progression. By elucidating its diverse regulatory mechanisms, we seek to encourage further research into the therapeutic implications of OPTN in cancer treatment and immunotherapy.

Our results confirmed that ST6GAL1 decreases the sensitivity of tumor cells to IFNG. This study describes a novel mechanism by which ST6GAL1 promotes the immune escape and malignant progression of CRC.

mTORC1 inhibition by rapamycin resensitizes the RAC1A159V tumors to anti-PD1 treatment by reversing effects of RAC1A159V mutation. These results demonstrate a mechanism of RAC1A159V-driven immune evasion and suggest an approach of combining the targeting of RAC1-mTOR signaling with immune checkpoint inhibitor for the treatment of a type of immune-cold tumors.

Furthermore, we identified that the tumor intrinsic IFNγ response and ascites-derived tumor-associated macrophages (TAMs) protect cancer cells from anoikis-mediated death within the IFNγ-rich ascites environment. Our study resolves temporal dynamics of disseminating tumor cells and highlights an ascites-driven, IFNγ program as a necessary pro-metastatic adaptation in the ovarian metastasis cascade.