Interleukin-1β Promotes Repair of the CNS
Open accessAbstract
Interleukin-1beta (IL-1beta) is a proinflammatory cytokine associated with the pathophysiology of demyelinating disorders such as multiple sclerosis and viral infections of the CNS. However, we demonstrate here that IL-1beta appears to promote remyelination in the adult CNS. In IL-1beta(-/-) mice, acute demyelination progressed similarly to wild-type mice and showed parallel mature oligodendrocyte depletion, microglia-macrophage accumulation, and the appearance of oligodendrocyte precursors. In contrast, IL-1beta(-/-) mice failed to remyelinate properly, and this appeared to correlate with a lack of insulin-like growth factor-1 (IGF-1) production by microglia-macrophages and astrocytes and to a profound delay of precursors to differentiate into mature oligodendrocytes. Thus, IL-1beta may be crucial to the repair of the CNS, presumably through the induction of astrocyte and microglia-macrophage-derived IGF-1.
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Accumulation of microglia and proliferation of OPC were not altered in IL-1β−/− mice.
“Interestingly, accumulation of microglia and proliferation of OPC were not altered in the IL-1β −/− mice.”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2001
The results sections report similar microglia-macrophage numbers and similar accumulation of NG2-positive oligodendrocyte progenitors in IL-1β-deficient and wild-type mice after five weeks of cuprizone exposure. The Discussion says progenitor accumulation could result from migration and/or local proliferation; it does not establish that OPC proliferation itself was unaltered. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIn the cuprizone model, IL-1β was gradually up-regulated from the first week of cuprizone intoxication, then strongly increased at week 3 and sustained on this level until week 6.
“In the cuprizone model IL-1β was gradually up-regulated from the first week of cuprizone intoxication, then strongly increased at week 3 and sustained on this level until week 6 (Mason et al., 2001).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2001
The section “Expression of IL-1β precedes an increase in IGF-1 expression” reports a dramatic increase in IL-1β mRNA at week 3 that was sustained through week 6. It does not specify that up-regulation began in the first week or increased gradually before week 3. (LLM, conf=0.85)
Experimental — accuracy not yet measuredDifferentiation of OPC and thus remyelination are dramatically reduced in the absence of IL-1β.
“In this study Mason and colleagues have shown that differentiation of OPC and thus, remyelination are dramatically reduced in absence of IL-1β”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2001
IL-1β did not display any impact on depletion of oligodendrocytes following cuprizone treatment.
“Additionally, IL-1β did not display any impact on depletion of oligodendrocytes following cuprizone treatment (Mason et al., 2001).”
From Glial response during cuprizone-induced de- and remyelination in the CNS: lessons learned (2014) · cites this paper as Mason et al., 2001
IL-1beta and TNF-alpha can be harmful for cerebral elements but also play beneficial roles in the inflammatory response.
“Such cytokines can thus be harmful for the cerebral elements (138) but they also play beneficial roles in the inflammatory response (161–163).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [163]
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- Authors
- Mason, J. L., Suzuki, K., Chaplin, D. D., & Matsushima, G. K.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Howard Hughes Medical Institute (US)
- ORCID
- Chaplin, David D.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2001-09-15
- Volume
- 21
- Issue
- 18
- Pages
- 7046-7052
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6762979
- OpenAlex
- W2158064024
- Cited by
- 502
- References
- 46
- Citations by year
- 2026: 10 · 2025: 7 · 2024: 11 · 2023: 13 · 2022: 13 · 2021: 14 · 2020: 22 · 2019: 20 · 2018: 10 · 2017: 15 · 2016: 18 · 2015: 20 · 2014: 23 · 2013: 21 · 2012: 17
- FWCI
- 17.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Multiple Sclerosis Society
- National Institutes of Health (5r29ns035372-05)
- National Institute of Neurological Disorders and Stroke (NS 24453, R01NS024453, NS-35372)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- IL-1β, remyelination, demyelination, oligodendrocyte differentiation, oligodendrocyte precursor cells, microglia/macrophages, astrocytes, insulin-like growth factor I, CNS repair, multiple sclerosis
- MeSH terms
- Animals, Antigens, Differentiation, Astrocytes, Cell Count, Central Nervous System, Chelating Agents, Corpus Callosum, Cuprizone, Demyelinating Diseases, Glutathione Transferase, Insulin-Like Growth Factor I, Interleukin-1, Isoenzymes, Macrophages, Mice, Inbred C57BL, Myelin Sheath, Oligodendroglia, Regeneration, RNA, Messenger, Stem Cells, Up-Regulation, Microglia, Mice, Knockout, Disease Progression, Mice, Glutathione S-Transferase pi
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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