ArticleCell reports2025
Alternatively spliced isoforms of IRF7 differentially regulate interferon expression to tune response to viral infection.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- HnRNPA2B1 tunes antimycobacterial immune responses in macrophages through alternative splicing ofInfection and immunity · 2026Article
- Review
- Nonsense-mediated decay controls a negative feedback loop in innate immune sensing.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Molecular arms races at the virus-host splicing interface and their pathogenic implications.Frontiers in microbiology · 2026Review
- HnRNPA2B1 tunes antimycobacterial immune responses in macrophages through alternative splicing ofbioRxiv : the preprint server for biology · 2025Article
- RNA processing in innate immunity: regulation by RNA-binding proteins.Trends in biochemical sciences · 2025Review
- Mechanism of electrothermal acupuncture in alleviating postherpetic neuralgia.Frontiers in neurologyArticle
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Authors and funding
10 authors.
Funding
Abstract
Interferon regulatory factor 7 (IRF7) is a master transcriptional regulator of innate immunity. IRF7 binds as a homodimer, or heterodimer with IRF3, to promoters of type I interferons (IFN-Is) to drive their expression, which activates expression of antiviral genes. Here, we demonstrate that alternative splicing of the first intron within the coding region of human IRF7 is regulated across immune tissues and in response to immunologic stimuli. Retention of this intron generates an alternative translation start site, resulting in an N-terminally extended form of the protein (exIRF7) compared to the canonical isoform (cIRF7). We find that exIRF7 has increased dimerization relative to cIRF7, uniquely activates expression of IFN-Is in response to double-stranded RNA (dsRNA) sensing, and controls viral infection to a greater extent than cIRF7. Thus, alternative splicing of IRF7 is a previously unrecognized mechanism by which human cells tune IRF7 function and the IFN response to control immune challenge.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.