Role of inflammasomes in multiple sclerosis and their potential as therapeutic targets
Open accessAbstract
Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS), and it remains the most common immune-mediated disorder affecting the CNS. While the cause of MS is unclear, the underlying pathomechanisms are thought to be either destruction by autoimmune T cells or dysfunction of myelin-producing cells. Recent advances have indicated that inflammasomes contribute the etiology of MS. Inflammasomes are multiprotein complexes of the innate immune response involved in the processing of caspase-1, the activation of pro-inflammatory cytokines interleukin (IL)-1β and IL-18 as well as the cell death-mediated mechanism of pyroptosis and the activation of the adaptive immune response. Here we review the literature to date on the role of different inflammasome signaling pathways in the pathogenesis of MS and how these pathways may be targeted to reduce deleterious inflammatory processes and improve outcomes in this patient population.
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Aberrant activation of the microglial NLRP3 inflammasome has been implicated in the onset and progression of multiple sclerosis.
“Aberrant activation of the microglial NLRP3 inflammasome has been implicated in the onset and progression of multiple sclerosis (MS), an autoimmune demyelinating disease of the CNS [192, 193].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [192]
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- Authors
- Govindarajan, V., de Rivero Vaccari, J. P., & Keane, R. W.
- Affiliations
- University of Miami (US)
- Corresponding author
- Keane, Robert W.
- Venue
- Journal of Neuroinflammation
- Published
- 2020-09-02
- Volume
- 17
- Issue
- 1
- Pages
- 260-260
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC7469327
- OpenAlex
- W3082497244
- Cited by
- 110
- References
- 103
- Citations by year
- 2026: 12 · 2025: 15 · 2024: 23 · 2023: 26 · 2022: 21 · 2021: 10 · 2020: 3
- FWCI
- 1.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS113969-01)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- multiple sclerosis, inflammasome, caspase-1, IL-1β, IL-18, pyroptosis, demyelination, autoimmune T cells, innate immunity, neuroinflammation, therapeutic target
- MeSH terms
- Animals, Humans, Immunologic Factors, Multiple Sclerosis, Signal Transduction, Cytokines, Caspases, Inflammasomes
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