ArticleCommunications biology2022
TOB1 attenuates IRF3-directed antiviral responses by recruiting HDAC8 to specifically suppress IFN-β expression.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 5 citations in OpenAlex.
- Article
- Reprogramming innate immunity through viral interference: A double-edged strategy for enhancing and containing gene therapies.Molecular therapy. Nucleic acids · 2026Review
- Single-cell transcriptome profiling reveals herpesviral manipulation of host processes in spleen of gibel carp infected with a Cyvirus cyprinidallo2.PLoS pathogens · 2026Article
- NAT10 Suppresses RNA Sensing Induced IFN-β Transactivation to Promote Viral Infection via Interfering with IRF3 Activities.bioRxiv : the preprint server for biology · 2025Article
- Identification of signature genes and relationship with immune cell infiltration in intervertebral disc degeneration.Frontiers in genetics · 2025Article
- A genome-wide CRISPR screening uncovers that TOB1 acts as a key host factor for FMDV infection via both IFN and EGFR mediated pathways.PLoS pathogens · 2024Article
- TOB1 modulates neutrophil phenotypes to influence gastric cancer progression and immunotherapy efficacy.Frontiers in immunology · 2024Article
- Effect of silencingFrontiers in plant science · 2023Article
- Regulation of IFNβ expression: focusing on the role of its promoter and transcription regulators.Frontiers in microbiology · 2023Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interferon regulatory factor 3 (IRF3) is a key transcription factor required for the secretion of type I interferons (IFN-α/β) and initiation of antiviral immune response. However, the negative feedback regulator of IRF3-directed antiviral response remains unknown. In this study, we demonstrated that viral infection induced the interaction of the transducer of ERBB2.1 (TOB1) with IRF3, which bound to the promoter region of Ifnb1 in macrophages. TOB1 inhibited Ifnb1 transcription by disrupting IRF3 binding and recruiting histone deacetylase 8 (HDAC8) to the Ifnb1 promoter region. Consequently, TOB1 attenuated IRF3-directed IFN-β expression in virus-infected macrophages. Tob1 deficiency enhanced antiviral response and suppressed viral replication in vivo. Thus, we identified TOB1 as a feedback inhibitor of host antiviral innate immune response and revealed a mechanism underlying viral immune escape.
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