ArticleNature communications2015
Breaking immune tolerance by targeting Foxp3(+) regulatory T cells mitigates Alzheimer's disease pathology.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 299 papers, 5 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
299 citing papers in PubMed, 5 syntheses or guidelines pooled it.
- Association between Periodontal Disease and Cognitive Impairment in Adults.International journal of environmental research and public health · 2023Pooled it
- Bibliometric analysis of global research trends on regulatory T cells in neurological diseases.Frontiers in neurology · 2023Pooled it
- The role of Bacillus Calmette-Guérin administration on the risk of dementia in bladder cancer patients: a systematic review and meta-analysis.Frontiers in aging neuroscience · 2023Pooled it
- Glatiramer Acetate Immunomodulation: Evidence of Neuroprotection and Cognitive Preservation.Cells · 2022Pooled it
- Pooled it
- Cell-based immunotherapy for neurodegenerative disease: A promising avenue.Neural regeneration research · 2026Article
- Review
- Neurodegenerative diseases and immune system: From pathogenic mechanism to therapy.Neural regeneration research · 2026Article
- Alzheimer's disease-cancer research (inception to 2025): trends, themes, translational pathways, and insights from highly cited studies.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Gamma-type immunoglobulin enhances phagocytosis of amyloid-beta fibrils by microglia.Neural regeneration research · 2026Article
- Adaptive immunity in the pathogenesis of neurodegeneration.Nature immunology · 2026Review
- Disruption of the brain-spleen axis impairs monocyte-microglia communication and accelerates disease progression in a mouse model of amyloidosis.Nature communications · 2026Article
- The Immune-Chemokine Axis in Alzheimer's Disease: Roles of Adaptive Immune System in Neuroinflammation and Disease Progression.Biomolecules · 2026Review
- Splenic treg-related immunoregulation in the spleen-brain axis of alzheimer's disease: mechanisms and translational strategies.Molecular biology reports · 2026Review
- Article
- Regulatory T cells in cancer and inflammation.Signal transduction and targeted therapy · 2026Review
- IL-1-mediated vitreous inflammation as an early indicator of retinal ganglion cell loss following acute optic nerve injury.Journal of neuroinflammation · 2026Article
- Therapeutic targeting of neuroimmune mechanisms in neurodegeneration.Nature reviews. Drug discovery · 2026Review
- Type I interferon drives T cell responses to amyloid beta in the central nervous system.Nature communications · 2026Article
- Microglial Innate Immune Memory: Implications and Research Advances in Central Nervous System Disorders.Current issues in molecular biology · 2026Review
239 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Alzheimer's disease (AD) is a neurodegenerative disorder in which chronic neuroinflammation contributes to disease escalation. Nevertheless, while immunosuppressive drugs have repeatedly failed in treating this disease, recruitment of myeloid cells to the CNS was shown to play a reparative role in animal models. Here we show, using the 5XFAD AD mouse model, that transient depletion of Foxp3(+) regulatory T cells (Tregs), or pharmacological inhibition of their activity, is followed by amyloid-β plaque clearance, mitigation of the neuroinflammatory response and reversal of cognitive decline. We further show that transient Treg depletion affects the brain's choroid plexus, a selective gateway for immune cell trafficking to the CNS, and is associated with subsequent recruitment of immunoregulatory cells, including monocyte-derived macrophages and Tregs, to cerebral sites of plaque pathology. Our findings suggest targeting Treg-mediated systemic immunosuppression for treating AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.