ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Differential requirement of histone acetylase and deacetylase activities for IRF5-mediated proinflammatory cytokine expression.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
- Inhibition of IRF5 hyperactivation protects from lupus onset and severity.The Journal of clinical investigation · 2020Trial
- Macrophage Immunometabolism in Epicardial Adipose Tissue and Obesity-Related Atrial Fibrillation.Journal of inflammation research · 2026Review
- HDAC inhibitors restore osteoimmune balance and bone regeneration via selective MAPK modulation in inflammatory bone disease.Stem cell research & therapy · 2025Article
- Characterization of T-bet expressing B cells in lupus patients indicates a putative prognostic and therapeutic value of these cells for the disease.Clinical and experimental immunology · 2025Article
- Interferon regulatory factor 5: a potential target for therapeutic intervention in inflammatory diseases.Frontiers in immunology · 2025Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- Interferon Regulatory Factor 5 Gene Polymorphisms and mRNA Expression Levels Are Associated with Neuromyelitis Optica Spectrum Disorder.Molecular neurobiology · 2024Article
- Intervening Effects and Molecular Mechanism of Quercitrin on PCV2-Induced Histone Acetylation, Oxidative Stress and Inflammatory Response in 3D4/2 Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Article
- Two Faces of Macrophages: Training and Tolerance.Biomedicines · 2021Review
- Tricarboxylic Acid (TCA) Cycle Intermediates: Regulators of Immune Responses.Life (Basel, Switzerland) · 2021Review
- Epigenetic Modifiers: Anti-Neoplastic Drugs With Immunomodulating Potential.Frontiers in immunology · 2021Review
- Foot-and-Mouth Disease Virus Capsid Protein VP1 Antagonizes TPL2-Mediated Activation of the IRF3/IFN-β Signaling Pathway to Facilitate the Virus Replication.Frontiers in immunology · 2020Article
- Advances and challenges in targeting IRF5, a key regulator of inflammation.The FEBS journal · 2019Review
- Epigenetic Mechanisms in Monocytes/Macrophages Regulate Inflammation in Cardiometabolic and Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
- IRF5 regulates unique subset of genes in dendritic cells during West Nile virus infection.Journal of leukocyte biology · 2019Article
- Association of interferon regulatory factor 5 (IRF5) gene polymorphisms with juvenile idiopathic arthritis.Clinical rheumatology · 2018Article
- Histone methylation and acetylation in macrophages as a mechanism for regulation of inflammatory responses.Journal of cellular physiology · 2018Review
- Epigenetic control of macrophage polarization: implications for targeting tumor-associated macrophages.Oncotarget · 2018Review
- Corrected and Republished from: The COP9 Signalosome Interacts with and Regulates Interferon Regulatory Factor 5 Protein Stability.Molecular and cellular biology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Recent evidence indicates a new role for histone deacetylases (HDACs) in the activation of genes governing the host immune response. Virus, along with other pathogenic stimuli, triggers an antiviral defense mechanism through the induction of IFN, IFN-stimulated genes, and other proinflammatory cytokines. Many of these genes have been shown to be regulated by transcription factors of the IFN regulatory factor (IRF) family. Recent studies from IRF5 knockout mice have confirmed a critical role for IRF5 in virus-induced type I IFN expression and proinflammatory cytokines IL-6, IL-12, and TNF-α; yet, little is known of the molecular mechanism of IRF5-mediated proinflammatory cytokine expression. In this study, we show that both HDACs and histone acetyltransferases (HATs) associate with IRF5, leading to alterations in its transactivation ability. Using the HDAC inhibitor trichostatin A, we demonstrate that ISRE, IFNA, and IL6 promoters require HDAC activity for transactivation and transcription, whereas TNFα does not. Mapping the interaction of corepressor proteins (HDAC1, silencing mediator of retinoid and thyroid receptor/nuclear corepressor of retinoid receptor, and Sin3a) and HATs to IRF5 revealed distinct differences, including the dependence of IRF5 phosphorylation on HAT association resulting in IRF5 acetylation. Data presented in this study support a mechanism whereby virus triggers the dynamic conversion of an IRF5-mediated silencing complex to that of an activating complex on promoters of target genes. These data provide the first evidence, to our knowledge, of a tightly controlled transcriptional mechanism whereby IRF5 regulates proinflammatory cytokine expression in conjunction with HATs and HDACs.
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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 OpenQuestion graph.