IFNAR1 (Interferon (alpha, beta and omega) receptor 1)

ENPP3 is a hypoxia-driven, cGAMP-targeting innate immune checkpoint in ccRCC. Its inhibition reactivates STING-dependent anti-tumor immunity, providing a strong preclinical rationale for targeting ENPP3 therapeutically.

Using this chimeric MHV68 virus, we demonstrate that lytic viral amplification must breach a threshold to trigger a potent virus-specific adaptive immune response. We propose that KSHV, through LANA, evades detection by repressing lytic viral replication to remain "below the radar" of adaptive immune defenses during host colonization.

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.

Notably, unlike ZIKV convalescent sera, Mi3-EDIII immune sera did not enhance DENV infection in human chronic myelogenous leukemia K562 cells, suggesting the absence of ADE-prone antibody induction. Our results demonstrate that Mi3-EDIII is a promising vaccine candidate against ZIKV infection and warrants further development.

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.

However, in xenograft tumor transplantation models, IFNAR1 KO cells formed larger tumors while STAT2 KO tumor cells formed smaller ones compared to parental tumor cells. These findings indicate that STAT2 promotes colorectal cancer growth through mechanisms independent of IFNAR1 signaling.

Patients with NSCLC with a low PPP2R2A/PD-L1 ratio respond better to immune checkpoint blockade (ICB). These findings underscore the therapeutic potential of ICB in treating PPP2R2A-deficient NSCLC while suggesting that PPP2R2A deficiency could serve as a biomarker for guiding ICB-based therapies.

In contrast, when the same T cells were boosted with a vaccine encoding antigen that stimulates through the TCR, the adoptively transferred T cells displayed improved persistence, tumour-specific endogenous cells expanded in parallel, and tumour cells carrying the antigen target were completely eradicated. Our findings underscore the need for further research into CAR-mediated vaccine boosting, how this differs mechanistically from TCR-mediated boosting, and the importance of engaging endogenous tumour-reactive T cells during vaccination to achieve long-term tumour control.

Males exhibit a more immunosuppressive profile, with higher levels of inhibitory immune markers and lower frequencies of functional NK cells. Our findings highlight the importance of incorporating sex-specific immune profiles into development of targeted therapies for advanced TC.

Normal human breast epithelium displays membrane-localized TYK2, whereas invasive breast tumors exhibit cytoplasmic TYK2. These findings uncover a TYK2-dependent mechanism by which ECM rigidity suppresses breast cancer metastasis and underscore the need for vigilant breast cancer screening in patients receiving TYK2 inhibitors.

Our new genetic model implicates ADAR1-mediated dsRNA signaling in gastric pre-neoplasia.

mRNA-LNP-mediated delivery of IFN-α-anti-GPC3 fusion protein achieves targeted in situ hepatic expression, significantly enhancing antitumor activity with a broad therapeutic window. This strategy offers a novel approach for precision immunotherapy in HCC, holding substantial potential for clinical translation.