ArticleScientific reports2024
Ischemic stroke outcome after promoting CD4+CD25+ Treg cell migration through CCR4 overexpression in a tMCAO animal model.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Regulatory T cells in stroke inflammation: Therapeutic perspectives.Neural regeneration research · 2026Article
- Neuroglia and immune cells play different roles in neuroinflammation and neuroimmune response in post-stroke neural injury and repair.Acta pharmacologica Sinica · 2026Review
- Systems-level analysis uncovers eight hub genes and a resveratrol-based therapeutic strategy for ischemic stroke.Frontiers in pharmacology · 2026Article
- Investigating the Mechanisms of Mitochondrial Dysfunction in Ischemic Stroke and Predicting Therapeutics Through Machine Learning and Integrated Bioinformatics.Current medicinal chemistry · 2026Article
- Microglial immunosurveillance after ischemic stroke: dynamic phenotypes, neurovascular interactions, and therapeutic opportunities.Frontiers in immunology · 2026Review
- Cellular Communication Networks Mediated by Microglia in Ischemic Stroke.CNS neuroscience & therapeutics · 2025Review
- CXCR4 and CXCR6 dually limit T cell entry into the polyomavirus-infected brain.Journal of neuroinflammation · 2025Article
- Regulatory T Cells for Stroke Recovery: A Promising Immune Therapeutic Strategy.CNS neuroscience & therapeutics · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The importance of neuroinflammation during the ischemic stroke has been extensively studied. The role of CD4+CD25+ regulatory T (Treg) cells during the recovery phase have shown infarct size reduction and functional improvement, possibly through the mitigation of inflammatory immune responses. We aimed to investigate the molecular factors involved in microglia-Treg cell communication that result in Treg trafficking. First, we observed the migration patterns of CD8+ (cytotoxic) T cells and Treg cells and then searched for chemokines released by activated microglia in an oxygen-glucose deprivation (OGD) model. The transwell migration assay showed increased migration into OGD media for both cell types, in agreement with the increase in chemokines involved in immune cell trafficking from the mouse chemokine profiling array. MSCV retrovirus was transduced to overexpress CCR4 in Treg cells. CCR4-overexpressed Treg cells were injected into the mouse transient middle cerebral artery occlusion (tMCAO) model to evaluate the therapeutic potential via the tetrazolium chloride (TTC) assay and behavioral tests. A general improvement in the prognosis of animals after tMCAO was observed. Our results suggest the increased mobility of CCR4-overexpressed Treg cells in response to microglia-derived chemokines in vitro and the therapeutic potential of Treg cells with increased mobility in cellular therapy.
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