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A hallmark of nervous system aging is a decline of white matter volume and function, but the underlying mechanisms leading to white matter pathology are unknown. In the present study, we found age-related alterations of oligodendrocyte cell state with a reduction in total oligodendrocyte density in aging murine white matter. Using single-cell RNA-sequencing, we identified interferon (IFN)-responsive oligodendrocytes, which localize in proximity to CD8(+) T cells in aging white matter. Absence of functional lymphocytes decreased the number of IFN-responsive oligodendrocytes and rescued oligodendrocyte loss, whereas T-cell checkpoint inhibition worsened the aging response. In addition, we identified a subpopulation of lymphocyte-dependent, IFN-responsive microglia in the vicinity of the CD8(+) T cells in aging white matter. In summary, we provide evidence that CD8(+) T-cell-induced, IFN-responsive oligodendrocytes and microglia are important modifiers of white matter aging.
SEEK ID: https://goeseek.gwdguser.de/studies/299
Z02 - Genomics and Bioinformatics Platform
Projects: TRR 274: Checkpoints of Central Nervous System Recovery
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Created: 3rd Aug 2026 at 12:17
Last updated: 3rd Aug 2026 at 12:44
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Projects: TRR 274: Checkpoints of Central Nervous System Recovery
Institutions: Universitätsmedizin Göttingen
Projects: CRC1002: Modulatory Units in Heart Failure, TRR 274: Checkpoints of Central Nervous System Recovery, SFB 1190: Compartmental Gates and Contact Sites in Cells
Web page: Not specified
https://rdp.sfb274.de/ (Research Data Platform) https://gepris.dfg.de/gepris/projekt/408885537 (DFG Gepris entry) The central nervous system (CNS) is a terminally differentiated tissue, where any insult carries a heightened risk - yet the tissue response to these insults is variable and can range from irreversible destruction to almost complete recovery. The rules that instruct these divergent outcomes are still unknown. The aim of this CRC is therefore to understand the biology of the multicellular ...
Programme: Sonderforschungsbereiche/Collaborative Research Centers
Public web page: https://www.sfb274.de/
Since the first funding period, Z02 has provided comprehensive support for all our research projects, from experimental design to bioinformatics data analysis. We specialize in bulk and single-cell genomic methods, including technologies like 10x Genomics and flow-cytometry based isolation methods. Additionally, we offer training on tissue preparation, single-cell sorting, and the use of 10x Genomics equipment to ensure high-quality data. By centralizing sample preparation, sequencing, and analysis, ...
Submitter: Camilla Giudici
Studies: A multi-modal single-cell and spatial expression map of metastatic breas..., CD8+ T cells induce interferon-responsive oligodendrocytes and microglia..., T cell-mediated microglial activation triggers myelin pathology in a mou...
Assays: Data availabilty, Expression profiling: MERFISH Spatial Transcriptomics (mouse), Expression profiling: scRNA-seq (mouse), Expression profiling: scRNA-seq (mouse)
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Submitter: Camilla Giudici
Assay type: Transcriptomics
Technology type: Sequencing
Investigation: Z02 - Genomics and Bioinformatics Platform
Organisms: Mouse
SOPs: No SOPs
Data files: CD8+ T cells induce interferon-responsive oligo...
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Study of oligodendrocytes and microglia in aging in a tissue-specific manner (white and gray matter) using the 10X single-cell RNA-sequencing platform. We also analyzed Rag1-deficient mice to study how the lack of mature T cells affect the age-dependent glial alterations that occur in the white matter.
Creators: None
Submitter: Camilla Giudici
Investigations: Z02 - Genomics and Bioinformatics Platform
Abstract (Expand)
Authors: Tuğberk Kaya, Nicola Mattugini, Lu Liu, Hao Ji, Ludovico Cantuti-Castelvetri, Jianping Wu, Martina Schifferer, Janos Groh, Rudolf Martini, Simon Besson-Girard, Seiji Kaji, Arthur Liesz, Ozgun Gokce, Mikael Simons
Date Published: 24th Oct 2022
Publication Type: Journal Article
DOI: 10.1038/s41593-022-01183-6
Citation: Nat Neurosci 25(11):1446-1457.
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https://orcid.org/0000-0002-9069-2594