Interferon-stimulated genes (ISGs) are the effectors of interferon (IFN) actions and play major roles in innate immune defense against microbial infection. During virus infection, ISGs impart antiviral actions to control virus replication and spread but can also contribute to disease pathology if their expression is unchecked[2]. Type I interferons (IFNs) facilitate cancer immunosurveillance, antitumor immunity and antitumor efficacy of conventional cell death-inducing therapies (chemotherapy/radiotherapy) as well as immunotherapy[3]. IFNs bind to their cognate receptors on the cellular membrane and activate the signaling pathway for transcriptional regulation of ISGs through Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway[4]. JAK-STAT signaling mediates almost all immune regulatory processes, including those that are involved in tumor cell recognition and tumor-driven immune escape. Antitumor immune responses are largely driven by STAT1 and STAT2 induction of type I and II IFNs and the downstream programs IFNs potentiate[5]. ChX710 could prime the type I interferon response to cytosolic DNA, which specific cellular ISGs, induces the ISRE promoter sequence, and the phosphorylation of IRF3.The treatment of ChX710 efficiently prime the cellular response to DNA transfection via STING as assessed by strong synergistic effects on IFN-β expression at both transcriptional and protein levels[6].
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