The DOI matches its Crossref record; 119 of the 119 references it cites were found in a registry or an index.
Microglia in Central Nervous System Inflammation and Multiple Sclerosis Pathology
Abstract
Microglia are the resident macrophages of the central nervous system (CNS). They have important physiological functions in maintaining tissue homeostasis but also contribute to CNS pathology. Microglia respond to changes in the microenvironment, and the resulting reactive phenotype can be very diverse, with both neuroinflammatory and neuroprotective properties, illustrating the plasticity of these cells. Recent progress in understanding the autoimmune neuroinflammatory disease multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis suggests major roles for microglia in the disease, which have drastically changed our view on the function of microglia in MS.
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In the citing paper
“Microglial cells and infiltrating monocytes/macrophages can have a dual role in MS lesions. They could contribute to myelin damage and lesion expansion, or they may have a protective role by clearing myelin debris, reducing inflammation and secreting regenerative factors promoting remyelination [48].”
From TREM2 activation on microglia promotes myelin debris clearance and remyelination in a model of multiple sclerosis (2020) · cites this paper as [48]
In the citing paper
“The pathophysiology of MS, especially its progressive forms, involves various cellular components, including microglia, the primary resident immune cells of the CNS.”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [8]
In the citing paper
“Microglia are highly adaptive and exhibit various functional states throughout different life stages and play critical roles in neuroinflammation, tissue repair, and neural homeostasis.”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [8]
In the citing paper
“As the primary resident immune cells of the CNS, microglia play a pivotal role in neuroinflammation, tissue repair, and neural homeostasis, and their activity is altered in MS (7–9).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [8]
In the citing paper
“In addition, microglia support the formation and elimination of synapses and promote the development of brain vasculature (8, 11, 14).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [8]
In the citing paper
“Various cellular components play a central role in the pathophysiology of progressive MS (8, 9).”
From The role of microglia in multiple sclerosis: implications for treatment with Bruton’s tyrosine kinase inhibitors (2025) · cites this paper as [8]
In the citing paper
“It involves the progressive loss of oligodendrocytes and neurons, resulting in motor and cognitive deficits [322, 326].”
From Microglia and monocytes in inflammatory CNS disease: integrating phenotype and function (2022) · cites this paper as [326]
In the citing paper
“Microglia are considered both pathogenic and protective during recovery from demyelination, but their precise role remains ill defined.”
From Microglia depletion exacerbates demyelination and impairs remyelination in a neurotropic coronavirus infection (2020) · cites this paper as [17]
In the citing paper
“Microglia are present and highly activated in lesions of demyelination where they have been described to have both harmful roles, such as production of cytotoxic cytokines, contribution to oxidative damage, and promotion of pathogenic T cell responses, as well as beneficial roles, including promotion of oligodendrocyte differentiation and clearance of myelin and cellular debris (14, 17–19).”
From Microglia depletion exacerbates demyelination and impairs remyelination in a neurotropic coronavirus infection (2020) · cites this paper as [17]
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Metadata
- Authors
- Voet, S., Prinz, M., & van Loo, G.
- Affiliations
- Vlaams Instituut voor Biotechnologie (BE)
- University of Freiburg (DE)
- ORCID
- Prinz, Marco
- Venue
- Trends in Molecular Medicine
- Publisher
- Elsevier BV
- Published
- 2019-02
- Volume
- 25
- Issue
- 2
- Pages
- 112-123
- ISSN
- 1471-4914 (ISSN-L)
- OpenAlex
- W2904871119
- Cited by
- 503
- References
- 119
- Citations by year
- 2026: 40 · 2025: 55 · 2024: 73 · 2023: 101 · 2022: 94 · 2021: 74 · 2020: 50 · 2019: 16
- FWCI
- 3.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Molecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Funders
- Fonds Wetenschappelijk Onderzoek
- Agentschap voor Innovatie door Wetenschap en Technologie
- Universiteit Gent
- Fondation Charcot
- Roman, Marga und Mareille Sobek Stiftung
- Bundesministerium für Bildung und Forschung
- Deutsche Forschungsgemeinschaft (SFB 992, SFB/TRR167, SFB1160)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- microglia, multiple sclerosis, experimental autoimmune encephalomyelitis, neuroinflammation, microglial plasticity, neuroprotection, tissue homeostasis
- MeSH terms
- Animals, Central Nervous System, Humans, Inflammation, Multiple Sclerosis, Microglia
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