The DOI matches its Crossref record; 122 of the 122 references it cites were found in a registry or an index.
Immunopathology of multiple sclerosis
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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“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).”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [77]
In the citing paper
“In addition to possible antigen-specific T cell-mediated inflammation, non-specific inflammation also contributes to myelin destruction in MS [77].”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [77]
In the citing paper
“Since currently available drugs insufficiently mitigate progression of neurodegeneration independent of the MS subtype (2), there is an urgent unmet clinical need for neuroprotective interventions.”
From MicroRNA-92a–CPEB3 axis protects neurons against inflammatory neurodegeneration (2023) · cites this paper as [2]
In the citing paper
“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]
In the citing paper
“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.”
From The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease (2019) · cites this paper as [4]
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Metadata
- 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
- FWCI
- 21.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- 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 › Clinical Neurology › 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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