Cited by 495Multiple Sclerosis Research StudiesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

Multiple sclerosis

Open access
Nylander, Alyssa, Hafler, David A.·2012·Journal of Clinical Investigation

Abstract

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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Research works printed but not linked: 3

  1. Lucchinetti C, Bruck W, Parisi J, Scheithauer B, Rodriguez M, Lassmann H. Heterogeneity of multiple sclerosis lesions: implications for the pathogenesis of demyelination. Ann Neurol. 2000; 47(6):707-717.
  2. Toyoda H, Formby B. Contribution of T cells to the development of autoimmune diabetes in the NOD mouse model. Bioessays. 1998;20(9):750-757.
  3. Raine CS, Cannella B, Hauser SL, Genain CP. Demyelination in primate autoimmune encepha- lomyelitis and acute multiple sclerosis lesions: a case for antigen-specific antibody mediation. Ann Neurol. 1999;46(2):144-160.

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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)
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
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

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