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USP18 lack in microglia causes destructive interferonopathy of the mouse brain
Open accessAbstract
Microglia are tissue macrophages of the central nervous system (CNS) that control tissue homeostasis. Microglia dysregulation is thought to be causal for a group of neuropsychiatric, neurodegenerative and neuroinflammatory diseases, called "microgliopathies". However, how the intracellular stimulation machinery in microglia is controlled is poorly understood. Here, we identified the ubiquitin-specific protease (Usp) 18 in white matter microglia that essentially contributes to microglial quiescence. We further found that microglial Usp18 negatively regulates the activation of Stat1 and concomitant induction of interferon-induced genes, thereby terminating IFN signaling. The Usp18-mediated control was independent from its catalytic activity but instead required the interaction with Ifnar2. Additionally, the absence of Ifnar1 restored microglial activation, indicating a tonic IFN signal which needs to be negatively controlled by Usp18 under non-diseased conditions. These results identify Usp18 as a critical negative regulator of microglia activation and demonstrate a protective role of Usp18 for microglia function by regulating the Ifnar pathway. The findings establish Usp18 as a new molecule preventing destructive microgliopathy.
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“Inappropriate upregulation of type I IFN signaling and ISG expression in the CNS have been linked to several interferonopathies including Aicardi-Goutieres syndrome and ubiquitin specific peptidase 18 (USP18)-deficiency in humans.”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [81]
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“which inhibits microglial activation by specifically blocking IFN-induced transcription”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Goldmann et al., 2015
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Metadata
- Authors
- Goldmann, T., Zeller, N., Raasch, J., Kierdorf, K., Frenzel, K., Ketscher, L., Basters, A., Staszewski, O., Brendecke, S. M., Spiess, A., Tay, T. L., Kreutz, C., Timmer, J., Mancini, G. M., Blank, T., Fritz, G., Biber, K., Lang, R., Malo, D., Merkler, D., Heikenwälder, M., Knobeloch, K., & Prinz, M.
- Affiliations
- University of Freiburg (DE)
- Erasmus MC (NL)
- University Medical Center Groningen (NL)
- Universitätsklinikum Erlangen (DE)
- McGill University (CA)
- University of Geneva (CH)
- Helmholtz Munich (DE)
- Corresponding author
- Prinz, Marco
- ORCID
- Venue
- The EMBO Journal
- Published
- 2015-04-20
- Volume
- 34
- Issue
- 12
- Pages
- 1612-1629
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- PMC
- PMC4475397
- OpenAlex
- W2097365950
- Cited by
- 223
- References
- 60
- Citations by year
- 2026: 14 · 2025: 19 · 2024: 15 · 2023: 23 · 2022: 11 · 2021: 35 · 2020: 22 · 2019: 25 · 2018: 15 · 2017: 22 · 2016: 14 · 2015: 7
- FWCI
- 10.33
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The EMBO Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- FreiDok plus (Universitätsbibliothek Freiburg) (submittedVersion)
- mediaTUM – the media and publications repository of the Technical University Munich (Technical University Munich) (submittedVersion)
- Site cant be reached (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- PuSH - Publication Server of Helmholtz Zentrum München (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- BMBF‐funded competence network of multiple sclerosis
- DFG (SFB 992, FOR1336, ZE 894/1‐1, PR 577/8‐1, KN590/3‐2 (SPP1365), KN590/1‐3)
- Fritz‐Thyssen Foundation
- Sobek Foundation
- Gemeinnützige Hertie Foundation
- ERA‐Net NEURON initiative “NEURO‐IFN”
- Canadian Institutes of Health Research (CTP‐87520)
- Swiss National Science Foundation (PP00P3_152928)
- Klaus‐Tschira Foundation
- Gebert‐Rüf Foundation
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- USP18, microglia, interferon signaling, STAT1, IFNAR2, IFNAR1, deubiquitination, microglial activation, neuroinflammation, interferonopathies, anti-inflammatory regulation
- MeSH terms
- Animals, Brain, Cloning, Molecular, Histological Techniques, Interferons, Microscopy, Fluorescence, Models, Neurological, Endopeptidases, Blotting, Western, Signal Transduction, Microglia, DNA Primers, Mice, Knockout, Statistics, Nonparametric, Ubiquitin Thiolesterase, Microarray Analysis, Microscopy, Electron, Transmission, Mice, Real-Time Polymerase Chain Reaction
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