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May 19, 2026Immunology0 citations

IFI16 /204 Promotes Dendritic Cell Activation and Anti‐Hepatocellular Carcinoma Efficacy via the STING – TBK1 – IRF3 Signalling Pathway

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ZLZhang LongHWHe WenjingHZHaitao Zhang

Key Points

  • This research investigates the role of IFI16 in dendritic cell activation and its anti-hepatocellular carcinoma effects through specific signaling pathways.
  • Demonstrated the effects of IFI16 on dendritic cell maturation and function.
  • Examined the activation of the STING-TBK1-IRF3 signaling pathway in response to IFI16.
  • Identified the potential of targeting IFI16 as a therapeutic strategy for hepatocellular carcinoma.
  • IFI16 significantly promotes dendritic cell maturation and functional activation.
  • Activation of the STING-TBK1-IRF3 pathway was essential for the antitumor immune response.
  • Targeting IFI16 represents a promising strategy for enhancing treatment efficacy in hepatocellular carcinoma.

Abstract

ABSTRACT IFI16 (the murine homologue is IFI204) is an intracellular double‐stranded DNA (dsDNA) pattern recognition receptor (PRR) that plays a crucial role in bridging innate and adaptive immunity. However, its function in dendritic cell (DC) activation and anti‐hepatocellular carcinoma (HCC) efficacy remains poorly characterised. This study demonstrates that IFI16 promotes DC maturation, functional activation and antitumor immunity. This effect occurs through activation of the STING–TBK1–IRF3 signalling pathway. Our findings establish IFI16 as a key molecule enabling DCs to sense dsDNA and initiate antitumor responses. Consequently, targeting IFI16 and its downstream STING–TBK1–IRF3 signalling pathway represents a potential therapeutic strategy for hepatocellular carcinoma.

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Cite This Study

Long et al. (2026) studied this question.

synapsesocial.com/papers/6a0bfe08166b51b53d3794a2https://doi.org/10.1111/imm.70152
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