ArticleCell & bioscience2026
USP30-AS1 functions as a post-transcriptional amplifier of interferon signalling to drive autoimmune pathogenesis.
Article in Cell & bioscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Interferon (IFN) signalling is essential for antiviral defence yet pathogenic in autoimmunity, however, the mechanisms orchestrating this duality remain poorly defined. Here, we identify USP30-AS1, a cytoplasmic long non-coding RNA (lncRNA) induced by type I IFN, as a pivotal post-transcriptional amplifier of innate immunity. We demonstrate that USP30-AS1 selectively enhances the mRNA stability of nucleic acid sensors. Moreover, USP30-AS1 preferentially stabilizes the majority of AU-rich element (ARE)-containing interferon-stimulated gene (ISG) mRNAs. USP30-AS1 executes this function independently of its antisense partner, USP30. The deletion of USP30-AS1 impaired IFN-β-mediated antiviral defence and suppressed pro-inflammatory cytokine production. Consistent with its role in amplifying immune responses, USP30-AS1 was markedly upregulated in human autoimmune diseases characterised by dysregulated IFN signalling, including systemic lupus erythematosus, rheumatoid arthritis, and dermatomyositis. Thus, our work unveils USP30-AS1 as a key regulator that fine-tunes the stability of nucleic acid sensors and ARE-containing immune transcripts, providing a direct mechanistic link between IFN signalling and post-transcriptional gene regulation. These findings establish USP30-AS1 as a critical rheostat for immune homeostasis and a promising therapeutic target for IFN-associated diseases.
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