IFNGR1 (Interferon Gamma Receptor 1)

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.

Moreover, indole-3-carbinol, interferon gamma-1b, and pretomanid (targeting IFNGR1) are potential keloid treatments...IFNGR1 was associated with the pathogenesis of keloids. Interferon gamma-1b targeting IFNGR1 might be a potential strategy for the treatment of keloids, and this discovery opened up a new direction for the treatment of keloids.

Functional validation revealed that BCAP31, a key risk gene, promotes CRC cell invasion and migration, while IFNGR1 demonstrated a protective role supported by Mendelian randomization (OR = 0.72). Our findings highlight the critical role of macrophage-driven immune dysregulation in CRC progression and propose BCAP31 as a potential therapeutic target, offering new insights into mitochondrial-immune crosstalk in the TME.

In the Chinese Han population, IFNGR1 genetic polymorphisms are closely associated with MAC-PD susceptibility, while IRF8 genetic polymorphisms are associated with MAB-PD susceptibility. Variants in IFNGR1 and IRF8 significantly affect the immune status and treatment outcomes of MAC-PD and MAB-PD patients, respectively.

Analysis of the TCGA database indicated that patients with high IFNGR1 expression had longer survival times than those with low expression (HR=0.87, 95%CI:0.77-0.98,P<0.05). In summary, the IFNGR1 -56 TG genotype is associated with an increased risk of breast cancer, and there is a positive correlation between IFNGR1 expression levels and the survival of breast cancer patients.