NLRP3 Plays a Critical Role in the Development of Experimental Autoimmune Encephalomyelitis by Mediating Th1 and Th17 Responses
Open accessAbstract
The interplay between innate and adaptive immunity is important in multiple sclerosis (MS). The inflammasome complex, which activates caspase-1 to process pro-IL-1beta and pro-IL-18, is rapidly emerging as a pivotal regulator of innate immunity, with nucleotide-binding domain, leucine-rich repeat containing protein family, pyrin domain containing 3 (NLRP3) (cryopyrin or NALP3) as a prominent player. Although the role of NLRP3 in host response to pathogen associated molecular patterns and danger associated molecular patterns is well documented, its role in autoimmune diseases is less well studied. To investigate the role of NLRP3 protein in MS, we used a mouse model of MS, experimental autoimmune encephalomyelitis (EAE). Nlrp3 expression was elevated in the spinal cords during EAE, and Nlrp3(-/-) mice had a dramatically delayed course and reduced severity of disease. This was accompanied by a significant reduction of the inflammatory infiltrate including macrophages, dendritic cells, CD4, and CD8(+) T cells in the spinal cords of the Nlrp3(-/-) mice, whereas microglial accumulation remained the same. Nlrp3(-/-) mice also displayed improved histology in the spinal cords with reduced destruction of myelin and astrogliosis. Nlrp3(-/-) mice with EAE produced less IL-18, and the disease course was similar to Il18(-/-) mice. Furthermore, Nlrp3(-/-) and Il18(-/-) mice had similarly reduced IFN-gamma and IL-17 production. Thus, NLRP3 plays a critical role in the induction of the EAE, likely through effects on capase-1-dependent cytokines which then influence Th1 and Th17.
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Inflammasome activation has an essential role in the progression of several neurological disorders like MS, AD, PPD, and NPS.
“In the CNS, inflammasome activation has been mainly linked to neuroinflammatory conditions. As example, it has an essential role in the progression of several neurological disorders like MS, AD, PPD, and NPS (132, 193–197).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [195]
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- Authors
- Gris, D., Ye, Z., Iocca, H. A., Wen, H., Craven, R. R., Gris, P., Huang, M., Schneider, M., Miller, S. D., & Ting, J. P.-Y.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Montreal Neurological Institute and Hospital (CA)
- Northwestern University (US)
- Corresponding author
- Gris, Denis
- Ye, Zhengmao
- Wen, Haitao
- Huang, Max
- Schneider, Monika
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-07
- Volume
- 185
- Issue
- 2
- Pages
- 974-981
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3593010
- OpenAlex
- W2096317294
- Cited by
- 429
- References
- 61
- Citations by year
- 2026: 20 · 2025: 17 · 2024: 29 · 2023: 33 · 2022: 32 · 2021: 38 · 2020: 36 · 2019: 34 · 2018: 29 · 2017: 28 · 2016: 27 · 2015: 20 · 2014: 20 · 2013: 24 · 2012: 21
- FWCI
- 8.47
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Multiple Sclerosis Society
- Multiple Sclerosis Society
- National Institutes of Health
- Canadian Institutes of Health Research
- National Institute of Neurological Disorders and Stroke (R01NS026543)
- 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
- NLRP3 inflammasome, experimental autoimmune encephalomyelitis, multiple sclerosis, Th1 cells, Th17 cells, IL-18, caspase-1, IL-17, interferon-gamma, myelin destruction, astrocyte activation, microglia, dendritic cells, CD4+ T cells, CD8+ T cells, NLRP3 knockout mice
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Enzyme-Linked Immunosorbent Assay, Female, Flow Cytometry, Gliosis, T-Lymphocytes, Helper-Inducer, Humans, Interferon-gamma, Male, Mice, Inbred C57BL, Multiple Sclerosis, Myelin Sheath, Severity of Illness Index, Spinal Cord, Immunoblotting, Mice, Knockout, Th1 Cells, Caspase 1, Interleukin-17, Interleukin-18, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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