ArticleCNS neuroscience & therapeutics2025
Repopulating Microglia Suppress Peripheral Immune Cell Infiltration to Promote Poststroke Recovery.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Spatiotemporally precise immune reprogramming: a new paradigm for next-generation neuroimmune therapy in ischemic stroke.Frontiers in neurology · 2026Review
- Single-cell and single-nucleus transcriptomics in ischemic stroke: cellular mechanisms and therapeutic implications.Frontiers in neurology · 2026Review
- Targeting microglia-mediated neuroinflammation in Alzheimer's disease: mechanisms and therapeutic approaches.Frontiers in immunology · 2026Review
- Repopulating Microglia Suppress Peripheral Immune Cell Infiltration to Promote Poststroke Recovery.CNS neuroscience & therapeutics · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
aimsSustained neuroinflammation following ischemic stroke impedes post-injury tissue repairment and neurological functional recovery. Developing innovative therapeutic strategies that simultaneously suppress detrimental inflammatory cascades and facilitate neurorestorative processes is critical for improving long-term rehabilitation outcomes.
methodsWe employed a microglia depletion-repopulation paradigm by administering PLX5622 for 7 days post-ischemia; followed by a 7-day withdrawal period to allow microglia repopulation. Single-cell transcriptomics, behavioral testing, cytokine arrays, flow cytometry, and immunofluorescence were used to assess the effects of microglia repopulation and delineate the transition of reshaped immune microenvironment.
resultsPLX5622 administration reshaped the poststroke immune microenvironment, promoting neurofunctional recovery. Repopulated microglia adopted a homeostatic phenotype, increasing homeostatic states by ~14.36% and reducing pro-inflammatory states by ~20.17%. This reshaped environment suppressed T cell exhaustion, limited neutrophil terminal differentiation, and promoted a phagocytic macrophage phenotype. Furthermore, we identified that these transitions in infiltrating immune cells may be driven by reduced chemokine production, enhanced blood-brain barrier (BBB) integrity, and transcriptional reprogramming.
conclusionTransient microglial depletion and repopulation via PLX5622 during the acute phase post stroke facilitate the recovery of neurological function. This immunomodulatory strategy offers a promising and clinically translationally relevant approach to enhance functional recovery following ischemic brain injury.
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