T cell infiltration in both human multiple system atrophy and a novel mouse model of the disease
Open accessAbstract
Multiple system atrophy (MSA) is a progressive neurodegenerative disorder characterized by abnormal accumulation of alpha-synuclein (α-syn) in oligodendrocytes accompanied by inflammation, demyelination, and subsequent synapse and neuronal loss. Little is known about the mechanisms of neurodegeneration in MSA. However, recent work has highlighted the important role of the immune system to the pathophysiology of other synuclein-related diseases such as Parkinson’s disease. In this study, we investigated postmortem brain tissue from MSA patients and control subjects for evidence of immune activation in the brain. We found a significant increase of HLA-DR+ microglia in the putamen and substantia nigra of MSA patient tissue compared to controls, as well as significant increases in CD3+, CD4+, and CD8+ T cells in these same brain regions. To model MSA in vivo, we utilized a viral vector that selectively overexpresses α-syn in oligodendrocytes (Olig001-SYN) with > 95% tropism in the dorsal striatum of mice, resulting in demyelination and neuroinflammation similar to that observed in human MSA. Oligodendrocyte transduction with this vector resulted in a robust inflammatory response, which included increased MHCII expression on central nervous system (CNS) resident microglia, and infiltration of pro-inflammatory monocytes into the CNS. We also observed robust infiltration of CD4 T cells into the CNS and antigen-experienced CD4 T cells in the draining cervical lymph nodes. Importantly, genetic deletion of TCR-β or CD4 T cells attenuated α-syn-induced inflammation and demyelination in vivo. These results suggest that T cell priming and infiltration into the CNS are key mechanisms of disease pathogenesis in MSA, and therapeutics targeting T cells may be disease modifying.
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T cell infiltration into the CNS and their interaction with microglia are key mechanisms of disease pathogenesis in MSA.
“These results suggest that T cell infiltration into the CNS and their interaction with microglia are key mechanisms of disease pathogenesis in MSA.301”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [301]
T cell infiltration alongside inflammatory microgliosis was observed both in postmortem brain tissues of MSA patients and in a virus-mediated mouse model of MSA.
“T cell infiltration alongside the inflammatory microgliosis was observed both in postmortem brain tissues of MSA patients and in a virus-mediated mouse model of MSA.301”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [301]
MSA mice with Tcrb (CD4 and CD8 T cell knockout) or Cd4 (CD4 T cell knockout) genetic deletion showed reduced inflammation and demyelination after exposure to syn.
“Moreover, MSA mice with Tcrb (CD4 and CD8 T cell knockout) or Cd4 (CD4 T cell knockout) genetic deletion showed reduced inflammation and demyelination after exposure to syn301”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [301]
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Self-citation
- Authors
- Williams, G. P., Marmion, D. J., Schonhoff, A. M., Jurkuvenaite, A., Won, W.-J., Standaert, D. G., Kordower, J. H., & Harms, A. S.
- Affiliations
- University of Alabama at Birmingham (US)
- Rush University Medical Center (US)
- Corresponding author
- Harms, Ashley S.
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 2020-01-29
- Volume
- 139
- Issue
- 5
- Pages
- 855-874
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- PMC
- PMC7181566
- OpenAlex
- W3004302491
- Cited by
- 102
- References
- 64
- Citations by year
- 2026: 10 · 2025: 10 · 2024: 12 · 2023: 16 · 2022: 18 · 2021: 20 · 2020: 16
- FWCI
- 6.76
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Acta Neuropathologica (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS107316)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Keywords
- multiple system atrophy, alpha-synuclein, T cell infiltration, neuroinflammation, demyelination, microglial activation, HLA-DR, oligodendrocytes, CD4+ T cells, mouse model, synucleinopathies, disease-modifying therapy
- MeSH terms
- Animals, Brain, Disease Models, Animal, Female, Humans, Male, Mice, Inbred C57BL, Neurons, Oligodendroglia, Parkinson Disease, T-Lymphocytes, Microglia, Multiple System Atrophy
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