Stage-specific roles of clonally expanded CD8+ T cells in regulating amyloid pathology in Alzheimer’s disease models
Open accessAbstract
Clonally expanded CD8+ T cells may contribute to Alzheimer’s disease (AD) pathology through interactions with brain-resident cells. However, the functional impact of AD-specific T cell receptor (TCR) clonotypes remains unclear. Here, we demonstrate that CD8+ T cells undergo clonal expansion in early-stage AD mouse models, AppNL-G-F and 5xFAD, and that their depletion reduces amyloid plaque accumulation. Expanded TCR-expressing CD8+ T cells preferentially infiltrate the brain, exacerbating plaque deposition. Moreover, brain-infiltrating CD8+ T cells impair microglial transition into disease-associated states, suppressing amyloid clearance via CCL5-CCR5 signaling. Pharmacological blockade of CCL5 attenuates amyloid deposition, whereas CCL5 administration aggravates pathology. Notably, T cell depletion at later disease stages exacerbates amyloid pathology, suggesting a temporal shift in their function. Early-stage CD8+ T cells exhibit cytotoxic and effector profiles, whereas late-stage cells acquire tissue-resident and exhausted phenotypes. This temporal switch—from pathogenic to protective roles—highlights the stage-specific contribution of CD8+ T cells to AD and their potential as therapeutic targets. Clonally expanded CD8 +T cells drive early Alzheimer’s pathology by suppressing microglial amyloid clearance through CCL5-CCR5 signaling, but later adopt protective roles, thereby revealing a stage-dependent functional transition.
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In mouse models, clonally expanded CD8-positive T cells interact dynamically with microglia: early CD8-positive T-cell activity can worsen amyloid pathology and constrain DAM-like microglial transition, whereas later T-cell states may become more tissue-resident or regulatory.
“In mouse models, clonally expanded CD8-positive T cells have also been shown to interact dynamically with microglia: early CD8-positive T-cell activity can worsen amyloid pathology and constrain DAM-like microglial transition, whereas later T-cell states may become more tissue-resident or regulatory.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [39]
CD28-positive microglia should be treated as part of a broader stage-dependent neuroimmune circuit involving microglia, plaques, and adaptive immune cells.
“These findings strengthen the rationale for treating CD28-positive microglia not as an isolated molecular curiosity, but as part of a broader stage-dependent neuroimmune circuit involving microglia, plaques, and adaptive immune cells [37,39].”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [39]
CD4-positive T cells in preclinical Alzheimer's disease show a type 2 helper profile and reactivity against Aβ-derived peptides, whereas MCI subjects show increased pro-inflammatory CD8-positive effector/TEMRA cells.
“Recent human work combining CyTOF, single-cell RNA sequencing, T-cell secretome analysis, and antigen-presentation assays reported that CD4-positive T cells in preclinical Alzheimer’s disease show a type 2 helper profile and reactivity against Aβ-derived peptides, whereas MCI subjects show increased pro-inflammatory CD8-positive effector/TEMRA cells.”
From Lymphoid-like Suppressive Microglia in Alzheimer’s Disease: A New Neuroimmune Regulatory Axis? (2026) · cites this paper as [39]
The Results describe effector CD8+ T cells in Alzheimer’s mouse models, not the claimed comparison between people with preclinical Alzheimer’s disease and those with MCI. Searches for CD4+ type 2 helper cells, Aβ-peptide reactivity, MCI/TEMRA cells, and the stated combination of human-study methods found no passage reporting those findings. The Results’ unsuccessful Aβ42 stimulation assay concerns mouse CD8+ T-cell receptors and does not resolve the claim about human CD4+ cells. (LLM, conf=0.76)
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- Authors
- Ohyagi, M., Ito, M., Iizuka-Koga, M., Mise-Omata, S., & Yoshimura, A.
- Affiliations
- Tokyo University of Science (JP)
- Kyushu University (JP)
- Corresponding author
- Ohyagi, Masaki
- Yoshimura, Akihiko
- Venue
- Nature Communications
- Published
- 2025-10-27
- Volume
- 16
- Issue
- 1
- Pages
- 9458-9458
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC12559718
- OpenAlex
- W4415585915
- Cited by
- 24
- References
- 57
- Citations by year
- 2026: 24
- FWCI
- 15.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nature Communications (publishedVersion, cc-by-nc-nd)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Takeda Science Foundation (2023049173)
- MEXT | Japan Society for the Promotion of Science (20K22789, 21K15473, 23KJ1876, 25K18841)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- Alzheimer's disease, CD8+ T cells, clonal expansion, amyloid plaques, microglial activation, T cell exhaustion, T cell depletion, T cell clonotypes, AppNL-G-F mice, 5xFAD mice, disease stage, neuroinflammation, amyloid clearance
- MeSH terms
- Alzheimer Disease, Animals, Brain, Disease Models, Animal, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Receptors, Antigen, T-Cell, Signal Transduction, Amyloid beta-Peptides, Microglia, CD8-Positive T-Lymphocytes, Chemokine CCL5, Receptors, CCR5, Mice, Plaque, Amyloid
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