IFNAR2 (Interferon Alpha And Beta Receptor Subunit 2)

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.

We additionally report that the translation of other immune receptor messenger RNAs, including TLR4, IFNAR1, and IFNGR2, is also controlled by uORFs. Thus, regulation of TNFR1 levels and possibly of other immune receptors emerges as a mechanism safeguarding against excessive immune responses and tissue damage.

These data indicate that GMAI-02 elicits robust humoral responses and confers protection against HAV challenge in the AG129 model. Our findings support conducting nonclinical efficacy assessments of hepatitis A vaccines in accessible mouse models, thereby reducing the reliance on nonhuman primates.

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.