E3 ligase RAD18 targets phosphorylated IRF3 to terminate <i>IFNB1</i> transcription – New Study
Nature Immunology, Published online: 29 August 2025; doi:10.1038/s41590-025-02256-x
IRF3 initiates type I IFN transcription, and this is required for host defense. Here, Chen and colleagues show that RAD18 terminates the transcriptional activity of IRF3 and subsequently promotes the autophagic degradation of IRF3.
Summary
A 2025 Nature Immunology study reveals a novel mechanism for regulating the immune response. While IRF3 initiates type I interferon (IFN) transcription, essential for host defense, Chen et al. found that RAD18 actively terminates IRF3’s transcriptional activity. Furthermore, RAD18 facilitates the autophagic degradation of IRF3, effectively dampening the IFN response. This discovery highlights the importance of RAD18 in preventing excessive inflammation and maintaining immune homeostasis by limiting IRF3 activity.
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