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IMMUNOLOGY OF MULTIPLE SCLEROSIS
Abstract
Multiple sclerosis (MS) develops in young adults with a complex predisposing genetic trait and probably requires an inciting environmental insult such as a viral infection to trigger the disease. The activation of CD4+ autoreactive T cells and their differentiation into a Th1 phenotype are a crucial events in the initial steps, and these cells are probably also important players in the long-term evolution of the disease. Damage of the target tissue, the central nervous system, is, however, most likely mediated by other components of the immune system, such as antibodies, complement, CD8+ T cells, and factors produced by innate immune cells. Perturbations in immunomodulatory networks that include Th2 cells, regulatory CD4+ T cells, NK cells, and others may in part be responsible for the relapsing-remitting or chronic progressive nature of the disease. However, an important paradigmatic shift in the study of MS has occurred in the past decade. It is now clear that MS is not just a disease of the immune system, but that factors contributed by the central nervous system are equally important and must be considered in the future.
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“Neurological deficits in MS patients result from two pathogenic events: acute inflammatory demyelination and axonal injury [150,151].”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [150]
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Metadata
- Authors
- Sospedra, M., & Martin, R.
- Affiliations
- National Institutes of Health (US)
- Cellular Immunology Section, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1400;
- ORCID
- Sospedra, Mireia
- Venue
- Annual Review of Immunology
- Publisher
- Annual Reviews
- Published
- 2005-04-01
- Volume
- 23
- Issue
- 1
- Pages
- 683-747
- ISSN
- 0732-0582 (ISSN-L)
- 1545-3278
- OpenAlex
- W2113291839
- Cited by
- 2,149
- References
- 362
- Citations by year
- 2026: 27 · 2025: 43 · 2024: 62 · 2023: 64 · 2022: 69 · 2021: 72 · 2020: 78 · 2019: 84 · 2018: 71 · 2017: 110 · 2016: 107 · 2015: 149 · 2014: 133 · 2013: 144 · 2012: 120
- FWCI
- 19.06
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annual Review of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- multiple sclerosis, autoimmunity, CD4+ T cells, Th1 cells, Th2 cells, regulatory T cells, natural killer cells, CD8+ T cells, complement system, autoantibodies, innate immunity, viral triggers, genetic susceptibility, relapsing-remitting disease, chronic progressive disease, central nervous system, neuroimmune interactions
- MeSH terms
- Autoantibodies, Autoantigens, Central Nervous System, HLA Antigens, Humans, Immunity, Innate, Immunogenetics, Infections, Multiple Sclerosis, Myelin Proteins, T-Lymphocyte Subsets, Cytokines, Models, Immunological, Molecular Mimicry, Chemokines, Genomics
About these checks
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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