Multiple sclerosis: a complicated picture of autoimmunity
Abstract
Understanding of autoimmune diseases, including multiple sclerosis, has expanded considerably in recent years. New insights have been provided by not only animal models but also studies of patients, often in conjunction with experimental therapies. It is accepted that autoimmune T cells mediate the early steps of new multiple sclerosis lesions, and although uncertainties remain about the specific targets of autoreactive T cells, several studies indicate myelin antigens. Recent findings obtained with both animal models and patients with multiple sclerosis indicate involvement of a T helper cell with a T(H)-17 phenotype, in contrast to previous data indicating that T helper type 1 cells are critical. Evidence has also been presented for CD8(+) and regulatory T cell populations, although their involvement remains to be established. Despite evidence supporting the idea that autoreactive T cells are involved in disease induction, cells of myeloid lineage, antibodies and complement as well as processes intrinsic to the central nervous system seem to determine the effector stages of tissue damage. Careful analysis of the alterations in immune processes should further advance knowledge of the relationship between the inflammatory component of this disease and the more diffuse degeneration of progressive multiple sclerosis.
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Multiple sclerosis is the prototypical neuroinflammatory disease in which demyelination is thought to result from a T-cell mediated autoimmune attack on myelin.
“Multiple sclerosis (MS) is the prototypical neuroinflammatory disease in which demyelination is thought to be related to a T-cell mediated autoimmune attack on myelin (McFarland and Martin, 2007).”
From The Pathobiology of Vascular Dementia (2013) · cites this paper as McFarland and Martin, 2007
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“Multiple sclerosis (MS) is the prototypical neuroinflammatory disease in which demyelination is thought to be related to a T cell mediated autoimmune attack on myelin (McFarland and Martin, 2007).”
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Inflammation and immunity in schizophrenia: implications for pathophysiology and treatment
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Single-cell profiling identifies myeloid cell subsets with distinct fates during neuroinflammation
Jordão, M. J. C., Sankowski, R., Brendecke, S. M., Sagar, Locatelli, G., Tai, Y.-H., Tay, T. L., Schramm, E., Armbruster, S., Hagemeyer, N., et al. (2019) · Science · doi:10.1126/science.aat7554 · Cited by 843 · see citing works
The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology
Rutsch, A., Kantsjö, J. B., & Ronchi, F. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.604179 · Cited by 821 · see citing works
Multiple sclerosis: risk factors, prodromes, and potential causal pathways
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Reactive astrocytes in neurodegenerative diseases
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Sankowski, R., Mader, S., & Valdés-Ferrer, S. I. (2015) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2015.00028 · Cited by 351 · see citing works
The development and function of regulatory T cells
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Diversity and plasticity of microglial cells in psychiatric and neurological disorders
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Role of microglial m1/m2 polarization in relapse and remission of psychiatric disorders and diseases
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Oligodendrocyte death results in immune-mediated CNS demyelination
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Anoctamin 2 identified as an autoimmune target in multiple sclerosis
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T cell infiltration in both human multiple system atrophy and a novel mouse model of the disease
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Galectin-3-Mediated Glial Crosstalk Drives Oligodendrocyte Differentiation and (Re)myelination
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Innate immune responses in central nervous system inflammation
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- Authors
- McFarland, H. F., & Martin, R.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- McFarland, Henry F
- ORCID
- McFarland, Henry F
- Venue
- Nature Immunology
- Published
- 2007-09
- Volume
- 8
- Issue
- 9
- Pages
- 913-919
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- OpenAlex
- W2085412596
- Cited by
- 985
- References
- 88
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 25 · 2023: 20 · 2022: 32 · 2021: 55 · 2020: 41 · 2019: 57 · 2018: 47 · 2017: 57 · 2016: 53 · 2015: 75 · 2014: 86 · 2013: 65 · 2012: 73
- FWCI
- 8.22
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nature Immunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Gemeinnützige Hertie-Stiftung
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- multiple sclerosis, autoimmunity, autoreactive T cells, myelin antigens, Th17 cells, Th1 cells, CD8+ T cells, regulatory T cells, myeloid cells, complement system, autoantibodies, neuroinflammation, progressive multiple sclerosis, demyelination, animal models
- MeSH terms
- Animals, Central Nervous System, T-Lymphocytes, Helper-Inducer, Humans, Inflammation, Multiple Sclerosis, Autoimmunity, T-Lymphocyte Subsets, Interleukin-17
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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