Cited by 2,215Multiple Sclerosis Research StudiesPsoriasis: Treatment and PathogenesisNeuroinflammation and Neurodegeneration Mechanisms

Immunopathology of multiple sclerosis

Dendrou, Calliope A., Fugger, Lars, Friese, Manuel A.·2015·Nature Reviews Immunology

Abstract

Two decades of clinical experience with immunomodulatory treatments for multiple sclerosis point to distinct immunological pathways that drive disease relapses and progression. In light of this, we discuss our current understanding of multiple sclerosis immunopathology, evaluate long-standing hypotheses regarding the role of the immune system in the disease and delineate key questions that are still unanswered. Recent and anticipated advances in the field of immunology, and the increasing recognition of inflammation as an important component of neurodegeneration, are shaping our conceptualization of disease pathophysiology, and we explore the potential implications for improved healthcare provision to patients in the future.

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Crossref · 10.1038/nri3871

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122 of 122 references verified0 citation errors · 0 not checkable

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  • Extensive infiltration and activation of peripheral and resident immune cells in MS suggests these cells are key mediators of lesion formation.

    “The extensive infiltration and activation of peripheral and resident immune cells in MS suggests these cells are key mediators of lesion formation [77, 210, 278] (Fig. 1j-l).”
  • In addition to possible antigen-specific T cell-mediated inflammation, non-specific inflammation also contributes to myelin destruction in MS.

    “In addition to possible antigen-specific T cell-mediated inflammation, non-specific inflammation also contributes to myelin destruction in MS [77].”
  • Both ASD and MS have been characterised by immunological abnormalities and dysfunctional myelination, at least in a subset of individuals.

    “Both conditions have been characterised by immunological abnormalities and dysfunctional myelination, at least in a subset of individuals [170,171].”

    From Vitamin D and Autism Spectrum Disorder: A Literature Review (2016) · cites this paper as [171]

  • Microglial gene expression changes may contribute to risk for autoimmune disorders of the central nervous system such as multiple sclerosis and lupus.

    “Furthermore, work from the past few years demonstrates that microglial gene expression changes during aging and may contribute to risk for AD (3) as well as autoimmune disorders of the central nervous system (CNS) such as multiple sclerosis [MS; reviewed in (4)] and lupus (5), but precisely how these cells contribute to risk for autoimmune disorders or AD remains unclear.”

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Authors
Dendrou, C. A., Fugger, L., & Friese, M. A.
Affiliations
  • John Radcliffe Hospital (GB)
  • Aarhus University Hospital (DK)
  • University Medical Center Hamburg-Eppendorf (DE)
Corresponding author
Fugger, Lars
Venue
Nature Reviews Immunology
Published
2015-08-07
Volume
15
Issue
9
Pages
545-558
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W1828576284
Cited by
2,215
References
122
Citations by year
2026: 117 · 2025: 177 · 2024: 243 · 2023: 230 · 2022: 252 · 2021: 272 · 2020: 257 · 2019: 216 · 2018: 201 · 2017: 159 · 2016: 83 · 2015: 5 · 2014: 1
FWCI
21.94
Type
journal article
Language
en
Open access
closed
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Wellcome Trust (100308/Z/12/Z, 100308)
  • Alan and Babette Sainsbury Charitable Fund
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
multiple sclerosis, immunopathology, genetic susceptibility, environmental triggers, neuroinflammation, neurodegeneration, immunomodulatory therapy, recurrence, disease progression
MeSH terms
Environmental Exposure, Humans, Inflammation, Multiple Sclerosis, Autoimmunity, Genetic Predisposition to Disease

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