ArticleJournal of neuroinflammation2022
CXCL13 expressed on inflamed cerebral blood vessels recruit IL-21 producing T
Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Experimental procedures for flow cytometry of wild-type mouse brain: a systematic review.Frontiers in immunology · 2023Pooled it
- Neurovascular dysfunction in the development and progression of neuroinflammatory diseases.Frontiers in cellular neuroscience · 2026Review
- A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage.International journal of general medicine · 2026Article
- Identification of post-translational modification-related biomarkers in ischemic stroke using bioinformatics and machine learning.Scientific reports · 2025Article
- Investigating the Potential Therapeutic Targeting of the JAK-STAT Pathway in Cerebrovascular Diseases: Opportunities and Challenges.Molecular neurobiology · 2025Review
- Chronic IL-21 drives neuroinflammation and promotes lipid accumulation in microglia.Immunity & ageing : I & A · 2025Article
- Temporal Transcriptomic Differences in Stroke Between Diabetic and Non-Diabetic Mice.Journal of molecular neuroscience : MN · 2025Article
- CD4Frontiers in immunology · 2025Review
- Mesangial cell-derived CircRNAs in chronic glomerulonephritis: RNA sequencing and bioinformatics analysis.Renal failure · 2024Article
- Chemokines play a role in nerve damage and neuroprotection in vascular dementia.IBRO neuroscience reports · 2024Review
- Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.Cellular & molecular biology letters · 2024Review
- Long noncoding RNA H19 knockdown promotes angiogenesis via IMP2 after ischemic stroke.CNS neuroscience & therapeutics · 2024Article
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- CCR2Cell reports · 2024Article
- Transcriptome analysis reveals the clinical significance of CXCL13 in Pan-Gyn tumors.Journal of cancer research and clinical oncology · 2024Article
- Article
- Analysis and Regulatory Mechanisms of Platelet-Related Genes in Patients with Ischemic Stroke.Cellular and molecular neurobiology · 2024Article
- The immunomodulatory mechanism of acupuncture treatment for ischemic stroke: research progress, prospects, and future direction.Frontiers in immunology · 2024Review
- Updates of the role of B-cells in ischemic stroke.Frontiers in cellular neuroscience · 2024Review
- Dietary Polyphenols Decrease Chemokine Release by Human Primary Astrocytes Responding to Pro-Inflammatory Cytokines.Pharmaceutics · 2023Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIschemic stroke is a leading cause of mortality worldwide, largely due to the inflammatory response to brain ischemia during post-stroke reperfusion. Despite ongoing intensive research, there have not been any clinically approved drugs targeting the inflammatory component to stroke. Preclinical studies have identified T cells as pro-inflammatory mediators of ischemic brain damage, yet mechanisms that regulate the infiltration and phenotype of these cells are lacking. Further understanding of how T cells migrate to the ischemic brain and facilitate neuronal death during brain ischemia can reveal novel targets for post-stroke intervention.
methodsTo identify the population of T cells that produce IL-21 and contribute to stroke, we performed transient middle cerebral artery occlusion (tMCAO) in mice and performed flow cytometry on brain tissue. We also utilized immunohistochemistry in both mouse and human brain sections to identify cell types and inflammatory mediators related to stroke-induced IL-21 signaling. To mechanistically demonstrate our findings, we employed pharmacological inhibitor anti-CXCL13 and performed histological analyses to evaluate its effects on brain infarct damage. Finally, to evaluate cellular mechanisms of stroke, we exposed mouse primary neurons to oxygen glucose deprivation (OGD) conditions with or without IL-21 and measured cell viability, caspase activity and JAK/STAT signaling.
resultsFlow cytometry on brains from mice following tMCAO identified a novel population of cells IL-21 producing CXCR5+ CD4+ ICOS-1+ T follicular helper cells (T
conclusionThese findings identify a novel mechanism for how pro-inflammatory T cells are recruited to the ischemic brain to propagate stroke damage and provide a potential new therapeutic target for stroke.
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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.