ArticleMetabolic brain disease2014
Treatment of experimental stroke with IL-10-producing B-cells reduces infarct size and peripheral and CNS inflammation in wild-type B-cell-sufficient mice.
Article in Metabolic brain disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 88 citations in OpenAlex.
- Regulatory T cells in stroke inflammation: Therapeutic perspectives.Neural regeneration research · 2026Article
- Regulatory B cells in the central nervous system: From immune regulation to neuroprotection.Neuroprotection (Chichester, England) · 2026Review
- Intraparenchymal B cell therapy protects neurological function and modulates local neuroinflammation in experimental hemorrhagic stroke.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Chemokine-receptor-guided B-cell immunity in cardiovascular disease.Basic research in cardiology · 2025Review
- Article
- B cells upregulate NMDARs, respond to extracellular glutamate, and express mature BDNF to protect the brain from ischemic injury.Neurobiology of disease · 2025Article
- The role of inflammation in Ischemic stroke: from biomarker to treatment.Frontiers in immunology · 2025Review
- Post stroke depression: pathogenesis and molecular mechanisms of natural product-based interventions.Frontiers in pharmacology · 2025Review
- Therapeutic Avenues to Modulate B-Cell Function in Patients With Cardiovascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Genetics of ischemic stroke functional outcome.Journal of neurology · 2024Review
- Updates of the role of B-cells in ischemic stroke.Frontiers in cellular neuroscience · 2024Review
- Role of Crosstalk between Glial Cells and Immune Cells in Blood-Brain Barrier Damage and Protection after Acute Ischemic Stroke.Aging and disease · 2023Review
- Review
- Bystanders or not? Microglia and lymphocytes in aging and stroke.Neural regeneration research · 2023Review
- B cell treatment promotes a neuroprotective microenvironment after traumatic brain injury through reciprocal immunomodulation with infiltrating peripheral myeloid cells.Journal of neuroinflammation · 2023Article
- Inflammation and immunomodulation in central nervous system injury - B cells as a novel therapeutic opportunity.Neurobiology of disease · 2023Review
- No evidence of oligoclonal bands, intrathecal immunoglobulin synthesis and B cell recruitment in acute ischemic stroke.PloS one · 2023Article
- Peripheral blood CD19 positive B lymphocytes increase after ischemic stroke and correlate with carotid atherosclerosis.Frontiers in neurology · 2023Article
- Intruders or protectors - the multifaceted role of B cells in CNS disorders.Frontiers in cellular neuroscience · 2023Review
- Immune regulation based on sex differences in ischemic stroke pathology.Frontiers in immunology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Clinical stroke induces inflammatory processes leading to cerebral and splenic injury and profound peripheral immunosuppression. IL-10 expression is elevated during major CNS diseases and limits inflammation in the brain. Recent evidence demonstrated that absence of B-cells led to larger infarct volumes and CNS damage after middle cerebral artery occlusion (MCAO) that could be prevented by transfer of IL-10(+) B-cells. The purpose of this study was to determine if the beneficial immunoregulatory effects on MCAO of the IL-10(+) B-cell subpopulation also extends to B-cell-sufficient mice that would better represent stroke subjects. CNS inflammation and infarct volumes were evaluated in male C57BL/6J (WT) mice that received either RPMI or IL-10(+) B-cells and underwent 60 min of middle cerebral artery occlusion (MCAO) followed by 96 h of reperfusion. Transfer of IL-10(+) B-cells markedly reduced infarct volume in WT recipient mice when given 24 h prior to or 4 h after MCAO. B-cell protected (24 h pre-MCAO) mice had increased regulatory subpopulations in the periphery, reduced numbers of activated, inflammatory T-cells, decreased infiltration of T-cells and a less inflammatory milieu in the ischemic hemispheres of the IL-10(+) B-cell-treated group. Moreover, transfer of IL-10(+) B-cells 24 h before MCAO led to a significant preservation of regulatory immune subsets in the IL-10(+) B-cell protected group presumably indicating their role in immunomodulatory mechanisms, post-stroke. Our studies are the first to demonstrate a major immunoregulatory role for IL-10(+) regulatory B-cells in preventing and treating MCAO in WT mice and also implicating their potential role in attenuating complications due to post-stroke immunosuppression.
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