The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Regulatory T cells delay disease progression in Alzheimer-like pathology
Abstract
Recent studies highlight the implication of innate and adaptive immunity in the pathophysiology of Alzheimer’s disease, and foster immunotherapy as a promising strategy for its treatment. Vaccines targeting amyloid-β peptide provided encouraging results in mouse models, but severe side effects attributed to T cell responses in the first clinical trial AN1792 underlined the need for better understanding adaptive immunity in Alzheimer’s disease. We previously showed that regulatory T cells critically control amyloid-β-specific CD4 + T cell responses in both physiological and pathological settings. Here, we analysed the impact of regulatory T cells on spontaneous disease progression in a murine model of Alzheimer’s disease. Early transient depletion of regulatory T cells accelerated the onset of cognitive deficits in APPPS1 mice, without altering amyloid-β deposition. Earlier cognitive impairment correlated with reduced recruitment of microglia towards amyloid deposits and altered disease-related gene expression profile. Conversely, amplification of regulatory T cells through peripheral low-dose IL-2 treatment increased numbers of plaque-associated microglia, and restored cognitive functions in APPPS1 mice. These data suggest that regulatory T cells play a beneficial role in the pathophysiology of Alzheimer’s disease, by slowing disease progression and modulating microglial response to amyloid-β deposition. Our study highlights the therapeutic potential of repurposed IL-2 for innovative immunotherapy based on modulation of regulatory T cells in Alzheimer’s disease. Increasing data implicate adaptive immunity in Alzheimer’s disease pathophysiology, but its involvement remains poorly defined. Using a mouse model, Dansokho et al. show that regulatory T cells slow cognitive decline and modulate the microglial response to amyloid deposition. The results support the therapeutic potential of regulatory T cell-based immunotherapy.
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Cites
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Meta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease
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Neuroinflammation in Alzheimer disease
Heneka, M. T., van der Flier, W. M., Jessen, F., Hoozemanns, J., Thal, D. R., Boche, D., Brosseron, F., Teunissen, C., Zetterberg, H., Jacobs, A. H., et al. (2025) · Nature Reviews Immunology · doi:10.1038/s41577-024-01104-7 · Cited by 638
Self-citationSolleiro-Villavicencio, H., & Rivas-Arancibia, S. (2018) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2018.00114 · Cited by 463
Antibiotics, gut microbiota, and Alzheimer’s disease
Angelucci, F., Cechova, K., Amlerova, J., & Hort, J. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1494-4 · Cited by 454
Peripheral and central immune system crosstalk in Alzheimer disease — a research prospectus
Bettcher, B. M., Tansey, M. G., Dorothée, G., & Heneka, M. T. (2021) · Nature Reviews Neurology · doi:10.1038/s41582-021-00549-x · Cited by 427
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Metadata
- Authors
- Dansokho, C., Ait Ahmed, D., Aid, S., Toly-Ndour, C., Chaigneau, T., Calle, V., Cagnard, N., Holzenberger, M., Piaggio, E., Aucouturier, P., & Dorothée, G.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2016-02-01
- Volume
- 139
- Issue
- 4
- Pages
- 1237-1251
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2257167523
- Cited by
- 359
- References
- 45
- FWCI
- 19.62
- Type
- journal article
- Language
- en
- Open access
- closed
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- Dansokho, C., Ait Ahmed, D., Aid, S., Toly-Ndour, C., Chaigneau, T., Calle, V., Cagnard, N., Holzenberger, M., Piaggio, E., Aucouturier, P., & Dorothée, G. (2016). Regulatory T cells delay disease progression in Alzheimer-like pathology. Brain. https://doi.org/10.1093/brain/awv408
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