Cited by 201Multiple Sclerosis Research StudiesNeuroinflammation and Neurodegeneration MechanismsNeurogenesis and neuroplasticity mechanisms

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CNS fibroblasts form a fibrotic scar in response to immune cell infiltration.

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Dorrier, Cayce E., Aran, Dvir, Haenelt, Ezekiel A., Sheehy, Ryan N., Hoi, Kimberly K., Pintarić, Lucija, Chen, Yanan, Lizama, Carlos O., Cautivo, Kelly M., Weiner, Geoffrey A., Popko, Brian, Fancy, Stephen P. J., Arnold, Thomas D., Daneman, Richard·2021·Nature Neuroscience

DOI 10.1038/s41593-020-00770-9PMC PMC7877789

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Abstract

Fibrosis is a common pathological response to inflammation in many peripheral tissues and can prevent tissue regeneration and repair. Here, we identified persistent fibrotic scarring in the CNS following immune cell infiltration in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. Using lineage tracing and single-cell sequencing in EAE, we determined that the majority of the fibrotic scar is derived from proliferative CNS fibroblasts, not pericytes or infiltrating bone marrow-derived cells. Ablating proliferating fibrotic cells using cell-specific expression of herpes thymidine kinase led to an increase in oligodendrocyte lineage cells within the inflammatory lesions and a reduction in motor disability. We further identified that interferon-gamma pathway genes are enriched in CNS fibrotic cells, and the fibrotic cell-specific deletion of Ifngr1 resulted in reduced fibrotic scarring in EAE. These data delineate a framework for understanding the CNS fibrotic response.

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Authors: Dorrier, C. E., Aran, D., Haenelt, E. A., Sheehy, R. N., Hoi, K. K., Pintarić, L., Chen, Y., Lizama, C. O., Cautivo, K. M., Weiner, G. A., Popko, B., Fancy, S. P. J., Arnold, T. D., & Daneman, R.
Affiliations: University of California San Diego (US)
Technion – Israel Institute of Technology (IL)
University of California, San Francisco (US)
Northwestern University (US)
Corresponding author: Arnold, Thomas D.
Daneman, Richard
ORCID: Aran, Dvir
Sheehy, Ryan N.
Pintarić, Lucija
Chen, Yanan
Lizama, Carlos O.
Cautivo, Kelly M.
Weiner, Geoffrey A.
Popko, Brian
Fancy, Stephen P. J.
Arnold, Thomas D.
Daneman, Richard
Venue: Nature Neuroscience
Publisher: Springer Science and Business Media LLC
Published: 2021-02
Volume: 24
Issue: 2
Pages: 234-244
ISSN: 1097-6256 (ISSN-L)
1546-1726
DOI: 10.1038/s41593-020-00770-9
PMC: PMC7877789
OpenAlex: W3128620467
Cited by: 199
References: 58
Citations by year: 2026: 23 · 2025: 35 · 2024: 39 · 2023: 44 · 2022: 33 · 2021: 25
FWCI: 23.65
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Nature Neuroscience (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion)
Funders: U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NS108651-01A1, NS034939, 5K08NS096192-02)
U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (GM007752)
National Multiple Sclerosis Society
UCSF Program for Breakthrough Biomedical Science
Topics: Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords: fibrotic scar, multiple sclerosis, experimental autoimmune encephalomyelitis, immune cell infiltration, fibroblast proliferation, meningeal fibrosis, oligodendrocyte lineage, interferon-gamma, IFNGR1, motor impairment, neuroinflammation
MeSH terms: Animals, Blood-Brain Barrier, Encephalomyelitis, Autoimmune, Experimental, Fibroblasts, Fibrosis, Oligodendroglia, Spinal Cord, Neutrophil Infiltration, Mice

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CNS fibroblasts form a fibrotic scar in response to immune cell infiltration.

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