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Il10 Deficiency Rebalances Innate Immunity to Mitigate Alzheimer-Like Pathology
Open accessAbstract
The impact of inflammation suppressor pathways on Alzheimer's disease (AD) evolution remains poorly understood. Human genetic evidence suggests involvement of the cardinal anti-inflammatory cytokine, interleukin-10 (IL10). We crossed the APP/PS1 mouse model of cerebral amyloidosis with a mouse deficient in Il10 (APP/PS1(+)Il10(-/-)). Quantitative in silico 3D modeling revealed activated Aβ phagocytic microglia in APP/PS1(+)Il10(-/-) mice that restricted cerebral amyloidosis. Genome-wide RNA sequencing of APP/PS1(+)Il10(-/-) brains showed selective modulation of innate immune genes that drive neuroinflammation. Il10 deficiency preserved synaptic integrity and mitigated cognitive disturbance in APP/PS1 mice. In vitro knockdown of microglial Il10-Stat3 signaling endorsed Aβ phagocytosis, while exogenous IL-10 had the converse effect. Il10 deficiency also partially overcame inhibition of microglial Aβ uptake by human Apolipoprotein E. Finally, the IL-10 signaling pathway was abnormally elevated in AD patient brains. Our results suggest that "rebalancing" innate immunity by blocking the IL-10 anti-inflammatory response may be therapeutically relevant for AD.
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“CCL20 (55), CSF3 (56) and IL10 (57) are associated with the inflammatory response in AD.”
From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [57]
In the citing paper
“Il10 deletion led to increased Aβ phagocytosis and increased CD68 reactivity in Aβ depositassociated microglia (133).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [133]
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“an independent study documented a role for the IL10-STAT3 pathway in mediating microglial Aβ phagocytosis (Guillot-Sestier et al., 2015).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Guillot-Sestier et al., 2015
In the citing paper
“Similarly, data examining the effects of microglia and inflammatory mediators on Aβ deposition in APP transgenic mice are mixed, with some studies demonstrating reduced and others exacerbated Aβ accumulation [120–122].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [121]
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Metadata
- Authors
- Guillot-Sestier, M.-V., Doty, K. R., Gate, D., Rodriguez, J., Leung, B. P., Rezai-Zadeh, K., & Town, T.
- Affiliations
- University of Southern California (US)
- Pennington Biomedical Research Center (US)
- Corresponding author
- Town, Terrence
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2015-02
- Volume
- 85
- Issue
- 3
- Pages
- 534-548
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC4352138
- OpenAlex
- W1999516517
- Cited by
- 363
- References
- 79
- Citations by year
- 2026: 19 · 2025: 18 · 2024: 30 · 2023: 26 · 2022: 33 · 2021: 34 · 2020: 39 · 2019: 33 · 2018: 28 · 2017: 41 · 2016: 43 · 2015: 19
- FWCI
- 23.34
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (1f31ns083339-01a1)
- National Institute on Aging (R00AG029726)
- National Institute of Neurological Disorders and Stroke (1F31NS083339-01A1, R01NS076794)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- IL-10, Alzheimer's disease, APP/PS1 mice, cerebral amyloidosis, microglia, amyloid-beta phagocytosis, innate immunity, neuroinflammation, STAT3 signaling, apolipoprotein E, synaptic integrity, cognitive impairment, anti-inflammatory cytokines
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Animals, Female, Humans, Immunity, Innate, Male, Mice, Inbred C57BL, Mice, Transgenic, Interleukin-10, Mice, Knockout, 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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