Il10 deficiency rebalances innate immunity to mitigate Alzheimer-like pathology
Guillot-Sestier MV, Doty KR, Gate D, Rodriguez J, Leung BP, Rezai-Zadeh K, Town T.. Neuron, 2015-01-22
Topic: Brain proteins, microglia and lab models
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.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Guillot-Sestier, M. V., Doty, K. R., Gate, D., Rodriguez, J., Leung, B. P., Rezai-Zadeh, K., et al. (2015). Il10 deficiency rebalances innate immunity to mitigate Alzheimer-like pathology. Neuron. https://doi.org/10.1016/j.neuron.2014.12.068
Vancouver
Guillot-Sestier MV, Doty KR, Gate D, Rodriguez J, Leung BP, Rezai-Zadeh K, et al. Il10 deficiency rebalances innate immunity to mitigate Alzheimer-like pathology. Neuron. 2015. doi:10.1016/j.neuron.2014.12.068. PMID: 25619654.
BibTeX
@article{guillotsestier2015-25619654,
author = {Guillot-Sestier, M. V. and Doty, K. R. and Gate, D. and Rodriguez, J. and Leung, B. P. and Rezai-Zadeh, K. and Town, T.},
title = {{Il10 deficiency rebalances innate immunity to mitigate Alzheimer-like pathology}},
journal = {Neuron},
year = {2015},
doi = {10.1016/j.neuron.2014.12.068},
pmid = {25619654},
url = {https://doi.org/10.1016/j.neuron.2014.12.068}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Quantitative in silico 3D modeling revealed activated Aβ phagocytic microglia in APP/PS1(+)Il10(-/-) mice that restricted cerebral amyloidosis.
- Our results suggest that "rebalancing" innate immunity by blocking the IL-10 anti-inflammatory response may be therapeutically relevant for AD.
Why it matters
In this mouse study, crossing the APP/PS1 model of cerebral amyloidosis with Il10-deficient mice restricted cerebral amyloidosis, preserved synaptic integrity, and mitigated cognitive disturbance. The authors suggest that blocking the IL-10 anti-inflammatory response may be therapeutically relevant for Alzheimer disease, but this is animal and in vitro work and has not been shown to treat or prevent the disease in people.
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Study details
- Evidence strengthLow
How this study scored 52/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neuron) |
| Journal's citation record | 4 / 4 | Neuron: journal h-index 689 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2015 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 363 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 27.9 citations a year over 13 year(s) since 2015 |
| Impact for its field and year | 4 / 6 | Cited 18.6× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 30 other studies in this library |
| Still being cited | 3 / 4 | Cited 67 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Terrence Town: h-index 67 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Southern California: institution h-index 1,521 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25619654) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 52 / 100 | — |
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Read the original
- DOI: 10.1016/j.neuron.2014.12.068
- PubMed: 25619654
- Original source →
- Free full text: PubMed Central →
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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