IFNAR2 (Interferon Alpha And Beta Receptor Subunit 2)

The combined data indicate that ErbB2, perhaps by driving micronuclei formation, has immunogenic properties that manifest in the form of increased T-cell infiltration and expansion, which can be exploited therapeutically by combining PD1-directed checkpoint blockade with ErbB2-targeted therapy.

The mechanism investigation demonstrated that several molecules, including Ticam1 (TRIF), Traf3, Mavs, and Ifnar2, were involved in promoting APC maturation and improving therapeutic efficacy of vaccines by activating innate immune pathways (TLR/NLR/RLR). In summary, this study provides a new DC-BC vaccine that has much better therapeutic efficacy and explores the underlying mechanism of why co-incubating DC and B cells improved the therapeutic efficacy.

P3, N=285, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting

P3, N=434, Active, not recruiting, Novartis Pharmaceuticals | Recruiting --> Active, not recruiting

RAB10 interacts with IFNAR1 to suppress the JAK1/STAT1 signaling pathway, thereby inhibiting M1 polarization and promoting M2 polarization of macrophages. Inhibition of RAB10, especially in combination with PD-L1 blockade, offers a promising strategy to enhance anti-tumor immunity and overcome therapeutic resistance in breast cancer.

Evading anti-viral responses is a key component of long-term viral persistence. In this work, we show that small noncoding RNAs expressed by multiple non-human primate γ-herpesviruses regulate anti-viral responses by directly targeting components of the type I interferon (IFN) signaling pathway.

This study revealed the presence of a UBE2H+ cell population within the pancreatic ductal cell niche and analyzed the inhibition of UBE2H on the immune microenvironment of pancreatic cancer through single-cell sequencing and in vivo experiments, providing important clues for the formation of "cold" tumors in pancreatic cancer and opening new directions for exploring new treatment strategies.

We present and validate a 17-MRRG prognostic model that links mitophagy receptors to glioma immunosuppression and clinical outcome, and identify IFNAR2 as a functional driver. These findings provide a rationale for incorporating MRRG profiling into prognostic assessment and therapeutic decision-making in glioma.

Our study reveals a distinct gut microbiota signature in CRC and suggests functional interactions between microbial dysbiosis and host inflammatory responses. These findings emphasize the potential of microbiota-based interventions and microbial metabolites as adjunctive strategies for the management of CRC.

Our findings revealed a complex and heterogeneous genetic background of IBC in the Tunisian population that might contribute to disease susceptibility and impact disease prognosis. The genetic features of IBC presented in this study provide valuable insights into the molecular mechanisms underlying the disease offering not only a deeper understanding within the context of Tunisia but also shedding light on its relevance to other North African populations characterized by similar epidemiological and genetic features.

This study provides novel insights into the role of macrophage Mertk-mediated efferocytosis and type I interferon response in the pathogenesis of heart failure. These findings highlight an unrecognized function of Mertk in pressure overload-induced cardiac remodeling and identify Ifn-β as a key downstream effector of Mertk in this pathological process.

This study proposes a glycolysis assessment strategy based on the interquartile range, which effectively addresses the limitations of previous scoring methods, including insufficient resolution and limited robustness. The proposed method enables more accurate quantification of intracellular glycolysis levels and facilitates fine-grained characterization of metabolic states. Furthermore, it identifies GPRC5A as a potential biomarker for the early diagnosis of gastric cancer. These findings enhance our understanding of metabolic reprogramming in gastric cancer and provide support for targeting the glycolytic pathway in therapeutic interventions.