ArticleJournal of immunology (Baltimore, Md. : 1950)2014
mTOR signaling inhibition modulates macrophage/microglia-mediated neuroinflammation and secondary injury via regulatory T cells after focal ischemia.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 176 citations in OpenAlex.
- Review
- Regulatory T cells in stroke inflammation: Therapeutic perspectives.Neural regeneration research · 2026Article
- Post-recanalization administration of rapamycin improves functional outcome and reduces infarct size in a rat model of ischemic stroke.Neuroprotection (Chichester, England) · 2026Article
- Peripheral Blood Regulatory T Cells and IL-6 are Associated with Cognitive Impairment After Acute Ischemic Stroke.Neuropsychiatric disease and treatment · 2026Article
- Regulatory T cells in intracerebral hemorrhage: mechanisms of immunomodulation and therapeutic potential.Frontiers in immunology · 2026Review
- Glioma‑associated microglia and macrophages as a potential target for mTOR inhibition in glioblastoma.Molecular medicine reports · 2025Article
- AAV hamartin gene therapy in a stochastic, cerebral mouse model of tuberous sclerosis type 1.Molecular therapy. Methods & clinical development · 2025Article
- A phenopushing platform to identify compounds that alleviate acute hypoxic stress by fast-tracking cellular adaptation.Nature communications · 2025Article
- Cachexia Alters Central Nervous System Morphology and Functionality in Cancer Patients.Journal of cachexia, sarcopenia and muscle · 2025Article
- Uncovering a new mechanism of ischemic stroke: a study of the association between γδ T cells and immunoinflammation.Frontiers in immunology · 2025Review
- Regulatory T Cells for Stroke Recovery: A Promising Immune Therapeutic Strategy.CNS neuroscience & therapeutics · 2025Review
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- TRPM7 Mediates Neuropathic Pain by Activating mTOR Signaling in Astrocytes after Spinal Cord Injury in Rats.Molecular neurobiology · 2024Article
- Targeting brain-peripheral immune responses for secondary brain injury after ischemic and hemorrhagic stroke.Journal of neuroinflammation · 2024Review
- Ketamine and the neurobiology of depression: Toward next-generation rapid-acting antidepressant treatments.Proceedings of the National Academy of Sciences of the United States of America · 2023Review
- Temporal changes in regulatory T cell subsets defined by the transcription factor Helios in stroke and their potential role in stroke-associated infection: a prospective case-control study.Journal of neuroinflammation · 2023Article
- Rapamycin Augmentation of Chronic Ketamine as a Novel Treatment for Complex Regional Pain Syndrome.Cureus · 2023Article
- Microglial phagocytosis dysfunction in stroke is driven by energy depletion and induction of autophagy.Autophagy · 2023Article
- Emerging Targets for Modulation of Immune Response and Inflammation in Stroke.Neurochemical research · 2023Review
- Regulatory T lymphocytes as a therapy for ischemic stroke.Seminars in immunopathology · 2023Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Signaling by the mammalian target of rapamycin (mTOR) plays an important role in the modulation of both innate and adaptive immune responses. However, the role and underlying mechanism of mTOR signaling in poststroke neuroinflammation are largely unexplored. In this study, we injected rapamycin, a mTOR inhibitor, by the intracerebroventricular route 6 h after focal ischemic stroke in rats. We found that rapamycin significantly reduced lesion volume and improved behavioral deficits. Notably, infiltration of γδ T cells and granulocytes, which are detrimental to the ischemic brain, was profoundly reduced after rapamycin treatment, as was the production of proinflammatory cytokines and chemokines by macrophages and microglia. Rapamycin treatment prevented brain macrophage polarization toward the M1 type. In addition, we also found that rapamycin significantly enhanced anti-inflammation activity of regulatory T cells (Tregs), which decreased production of proinflammatory cytokines and chemokines by macrophages and microglia. Depletion of Tregs partially elevated macrophage/microglia-induced neuroinflammation after stroke. Our data suggest that rapamycin can attenuate secondary injury and motor deficits after focal ischemia by enhancing the anti-inflammation activity of Tregs to restrain poststroke neuroinflammation.
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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.