ArticleJournal of neuroinflammation2014
Interferon regulatory factor (IRF) 3 is critical for the development of experimental autoimmune encephalomyelitis.
Article in Journal of neuroinflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Microglia regulate myelin clearance and cholesterol metabolism after demyelination via interferon regulatory factor 5.Cellular and molecular life sciences : CMLS · 2025Article
- Interferon Regulatory Factors as a Potential Therapeutic Target for Neuroinflammation: A Focus on Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Toll-like receptors in pathogenesis of neurodegenerative diseases and their therapeutic potential.Immunity, inflammation and disease · 2023Review
- Botanically-Derived ΔMolecules (Basel, Switzerland) · 2022Article
- Proximal and Distal Regions of Pathogenic Th17 Related Chromatin Loci Are Sequentially Accessible During Pathogenicity of Th17.Frontiers in immunology · 2022Article
- Review
- Context Is Key: Delineating the Unique Functions of IFNα and IFNβ in Disease.Frontiers in immunology · 2020Review
- Amlexanox attenuates experimental autoimmune encephalomyelitis by inhibiting dendritic cell maturation and reprogramming effector and regulatory T cell responses.Journal of neuroinflammation · 2019Article
- The Evolving Mechanisms of Action of Glatiramer Acetate.Cold Spring Harbor perspectives in medicine · 2019Review
- Regulation of Toll-Like Receptor (TLR) Signaling Pathway by Polyphenols in the Treatment of Age-Linked Neurodegenerative Diseases: Focus on TLR4 Signaling.Frontiers in immunology · 2019Review
- Interferon regulatory factors 3 and 7 have distinct roles in the pathogenesis of alphavirus encephalomyelitis.The Journal of general virology · 2019Article
- Revisiting the role of IRF3 in inflammation and immunity by conditional and specifically targeted gene ablation in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Regulation of TLR signaling pathways by microRNAs: implications in inflammatory diseases.Central-European journal of immunology · 2018Review
- Therapeutic Targeting of IRFs: Pathway-Dependence or Structure-Based?Frontiers in immunology · 2018Review
- Review
- Glatiramer acetate treatment negatively regulates type I interferon signaling.Neurology(R) neuroimmunology & neuroinflammation · 2015Article
- Role of TRIF Small Interference RNA (siRNA) in Chronic Experimental Allergic Encephalomyelitis (EAE).Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Transcriptome sequencing of microglial cells stimulated with TLR3 and TLR4 ligands.BMC genomics · 2015Article
- Dual RNA sequencing reveals the expression of unique transcriptomic signatures in lipopolysaccharide-induced BV-2 microglial cells.PloS one · 2015Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundExperimental autoimmune encephalomyelitis (EAE) is an animal model of autoimmune inflammatory demyelination that is mediated by Th1 and Th17 cells. The transcription factor interferon regulatory factor 3 (IRF3) is activated by pathogen recognition receptors and induces interferon-β production.
methodsTo determine the role of IRF3 in autoimmune inflammation, we immunised wild-type (WT) and irf3(-/-) mice to induce EAE. Splenocytes from WT and irf3(-/-) mice were also activated in vitro in Th17-polarising conditions.
resultsClinical signs of disease were significantly lower in mice lacking IRF3, with reduced Th1 and Th17 cells in the central nervous system. Peripheral T-cell responses were also diminished, including impaired proliferation and Th17 development in irf3(-/-) mice. Myelin-reactive CD4+ cells lacking IRF3 completely failed to transfer EAE in Th17-polarised models as did WT cells transferred into irf3(-/-) recipients. Furthermore, IRF3 deficiency in non-CD4+ cells conferred impairment of Th17 development in antigen-activated cultures.
conclusionThese data show that IRF3 plays a crucial role in development of Th17 responses and EAE and warrants investigation in human multiple sclerosis.
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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.