Multiple sclerosis
Open accessAbstract
Multiple sclerosis (MS) is a multifocal demyelinating disease with progressive neurodegeneration caused by an autoimmune response to self-antigens in a genetically susceptible individual. While the formation and persistence of meningeal lymphoid follicles suggest persistence of antigens to drive the continuing inflammatory and humoral response, the identity of an antigen or infectious agent leading to the oligoclonal expansion of B and T cells is unknown. In this review we examine new paradigms for understanding the immunopathology of MS, present recent data defining the common genetic variants underlying disease susceptibility, and explore how improved understanding of immune pathway disruption can inform MS prognosis and treatment decisions.
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Multiple sclerosis is a chronic inflammatory and neurodegenerative disease of the central nervous system with a possible autoimmune etiology.
“MS is a chronic inflammatory and neurodegenerative disease of CNS with a possible autoimmune etiology [149].”
From Beneficial Effects of Spirulina Consumption on Brain Health (2022) · cites this paper as [149]
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Antibodies from Inflamed Central Nervous System Tissue Recognize Myelin Oligodendrocyte Glycoprotein
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Lack of TIM-3 Immunoregulation in Multiple Sclerosis
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Genome-wide association study of severity in multiple sclerosis
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Chromatin remodeling: a marriage between two families?
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Evidence for VAV2 and ZNF433 as susceptibility genes for multiple sclerosis
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A case of multiple sclerosis presenting with inflammatory cortical demyelination
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The plasticity of human Treg and Th17 cells and its role in autoimmunity
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“74,75,91 These results suggest that a strong tissue inflammatory response is involved in MS and emphasizes that the tissue-specific gene program centered on the AP-1 family may be a novel MS-specific therapeutic target.”
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Ten years of proteomics in multiple sclerosis
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- Authors
- Nylander, A., & Hafler, D. A.
- Affiliations
- Biogen (United States) (US)
- Corresponding author
- Hafler, David A.
- Venue
- Journal of Clinical Investigation
- Published
- 2012-04-02
- Volume
- 122
- Issue
- 4
- Pages
- 1180-1188
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3314452
- OpenAlex
- W4252639669
- Cited by
- 495
- References
- 116
- Citations by year
- 2026: 8 · 2025: 18 · 2024: 19 · 2023: 17 · 2022: 30 · 2021: 28 · 2020: 37 · 2019: 45 · 2018: 40 · 2017: 33 · 2016: 56 · 2015: 57 · 2014: 45 · 2013: 53 · 2012: 8
- FWCI
- 7.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Yale University
- Nancy Taylor Foundation for Chronic Diseases
- National Institutes of Health
- Raymond and Beverly Sackler Institute for Biological, Physical and Engineering Sciences, Yale University
- National Cancer Institute (CA1061-A-18)
- National Institute of General Medical Sciences (TG-T32GM07205, T32GM007205)
- National Institute of Allergy and Infectious Diseases (R01 AI09156, U19 AI08999, P01 AI03967, F32AI009156, U19 AI07035, P01 AI04575, P01 AI07374)
- National Institute of Neurological Disorders and Stroke (RC2 NS07034)
- 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, demyelination, neurodegeneration, autoimmunity, autoantigens, oligoclonal expansion, immunopathology, genetic susceptibility, prognosis, treatment decision-making
- MeSH terms
- Alleles, Autoantigens, Autoimmune Diseases, Forecasting, Humans, Lymphocyte Activation, Meninges, Multiple Sclerosis, B-Lymphocyte Subsets, T-Lymphocyte Subsets, Cytokines, Models, Immunological, Genetic Predisposition to Disease, T-Lymphocytes, Regulatory, Forkhead Transcription Factors, Genome-Wide Association Study, Costimulatory and Inhibitory T-Cell Receptors
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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