ArticleJournal of neuroinflammation2012
Interferon regulatory factor 8/interferon consensus sequence binding protein is a critical transcription factor for the physiological phenotype of microglia.
Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 84 citations in OpenAlex.
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- Repeated LPS induces training and tolerance of microglial responses across brain regions.Journal of neuroinflammation · 2024Article
- The Implications of Microglial Regulation in Neuroplasticity-Dependent Stroke Recovery.Biomolecules · 2023Review
- Transcriptomic analysis reveals the immune response of human microglia to a soy protein and collagen hybrid bioscaffold.Heliyon · 2023Article
- The Role of Vitamin D in Alzheimer's Disease: A Transcriptional Regulator of Amyloidopathy and Gliopathy.Biomedicines · 2022Article
- The Role of Microglia in Neuroinflammation of the Spinal Cord after Peripheral Nerve Injury.Cells · 2022Review
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- Transcriptional and epigenetic regulation of microglia in maintenance of brain homeostasis and neurodegeneration.Frontiers in molecular neuroscience · 2022Review
- Lack of Interferon (IFN) Regulatory Factor 8 Associated with Restricted IFN-γ Response Augmented Japanese Encephalitis Virus Replication in the Mouse Brain.Journal of virology · 2021Article
- The role of interferon regulatory factor 8 for retinal tissue homeostasis and development of choroidal neovascularisation.Journal of neuroinflammation · 2021Article
- Mapping the Plasticity of Morphology, Molecular Properties and Function in Mouse Primary Microglia.Frontiers in cellular neuroscience · 2021Article
- Impact of ambient temperature on inflammation-induced encephalopathy in endotoxemic mice-role of phosphoinositide 3-kinase gamma.Journal of neuroinflammation · 2020Article
- Dynamic Responses of Microglia in Animal Models of Multiple Sclerosis.Frontiers in cellular neuroscience · 2020Article
- Article
- Reverse genetic screen reveals that Il34 facilitates yolk sac macrophage distribution and seeding of the brain.Disease models & mechanisms · 2019Article
- Transcriptional mechanism of IRF8 and PU.1 governs microglial activation in neurodegenerative condition.Protein & cell · 2019Article
- Long Noncoding RNA Expression Profile in BV2 Microglial Cells Exposed to Lipopolysaccharide.BioMed research international · 2019Article
- Allograft Inflammatory Factor-1 Governs Hematopoietic Stem Cell Differentiation Into cDC1 and Monocyte-Derived Dendritic Cells Through IRF8 and RelBFrontiers in immunology · 2019Article
- A state-of-the-art perspective on microgliopathic pain.Open biology · 2018Review
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundRecent fate-mapping studies establish that microglia, the resident mononuclear phagocytes of the CNS, are distinct in origin from the bone marrow-derived myeloid lineage. Interferon regulatory factor 8 (IRF8, also known as interferon consensus sequence binding protein) plays essential roles in development and function of the bone marrow-derived myeloid lineage. However, little is known about its roles in microglia.
methodsThe CNS tissues of IRF8-deficient mice were immunohistochemically analyzed. Pure microglia isolated from wild-type and IRF8-deficient mice were studied in vitro by proliferation, immunocytochemical and phagocytosis assays. Microglial response in vivo was compared between wild-type and IRF8-deficient mice in the cuprizon-induced demyelination model.
resultsOur analysis of IRF8-deficient mice revealed that, in contrast to compromised development of IRF8-deficient bone marrow myeloid lineage cells, development and colonization of microglia are not obviously affected by loss of IRF8. However, IRF8-deficient microglia demonstrate several defective phenotypes. In vivo, IRF8-deficient microglia have fewer elaborated processes with reduced expression of IBA1/AIF1 compared with wild-type microglia, suggesting a defective phenotype. IRF8-deficient microglia are significantly less proliferative in mixed glial cultures than wild-type microglia. Unlike IRF8-deficient bone marrow myeloid progenitors, exogenous macrophage colony stimulating factor (colony stimulating factor 1) (M-CSF (CSF1)) restores their proliferation in mixed glial cultures. In addition, IRF8-deficient microglia exhibit an exaggerated growth response to exogenous granulocyte-macrophage colony stimulating factor (colony stimulating factor 2) (GM-CSF (CSF2)) in the presence of other glial cells. IRF8-deficient microglia also demonstrate altered cytokine expressions in response to interferon-gamma and lipopolysaccharide in vitro. Moreover, the maximum phagocytic capacity of IRF8-deficient microglia is reduced, although their engulfment of zymosan particles is not overtly impaired. Defective scavenging activity of IRF8-deficient microglia was further confirmed in vivo in the cuprizone-induced demyelination model in mice.
conclusionsThis study is the first to demonstrate the essential contribution of IRF8-mediated transcription to a broad range of microglial phenotype. Microglia are distinct from the bone marrow myeloid lineage with respect to their dependence on IRF8-mediated transcription.
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