ArticleThe Journal of experimental medicine2014
T cell-derived interleukin (IL)-21 promotes brain injury following stroke in mice.
Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
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Who cites it
70 citing papers in PubMed, 106 citations in OpenAlex.
- Targeting CD4⁺ T cell infiltration: mechanisms and therapeutic insights into CD4⁺ T cell transmigration across the blood-brain barrier in acute ischemic stroke.Fluids and barriers of the CNS · 2026Review
- Flow Cytometric Profiling Reveals Platelet Dysfunction and Impaired Immune Communication in Acute and Chronic Cerebrovascular Disease.Journal of clinical laboratory analysis · 2026Article
- Hspa8 modulation of immune responses mitigates ischemic brain injury.Genes and immunity · 2026Article
- Rab7a is required to degrade select blood-brain barrier junctional proteins after ischemic stroke.Acta neuropathologica communications · 2025Article
- CD8Cellular & molecular immunology · 2025Article
- Chronic IL-21 drives neuroinflammation and promotes lipid accumulation in microglia.Immunity & ageing : I & A · 2025Article
- Repair-associated macrophages increase after early-phase microglia attenuation to promote ischemic stroke recovery.Nature communications · 2025Article
- Neural repair mechanisms after ischemic stroke.Inflammation and regeneration · 2025Review
- Novel co-culture model of T cells and midbrain organoids for investigating neurodegeneration in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Article
- CD4Frontiers in immunology · 2025Review
- Chemokine CXCL13-CXCR5 signaling in neuroinflammation and pathogenesis of chronic pain and neurological diseases.Cellular & molecular biology letters · 2024Review
- The roles of Th cells in myocardial infarction.Cell death discovery · 2024Review
- SHARPIN contributes to sevoflurane-induced neonatal neurotoxicity through up-regulating HMGB1 to repress M2 like-macrophage polarization.Metabolic brain disease · 2024Article
- Genetic insights into the relationship between immune cell characteristics and ischemic stroke: A bidirectional Mendelian randomization study.European journal of neurology · 2024Article
- Article
- Protective effects of fecal microbiota transplantation against ischemic stroke and other neurological disorders: an update.Frontiers in immunology · 2024Review
- Perspective from single-cell sequencing: Is inflammation in acute ischemic stroke beneficial or detrimental?CNS neuroscience & therapeutics · 2024Review
- Aflatoxin BBrain sciences · 2023Article
- The Dual Role of Autophagy in Postischemic Brain Neurodegeneration of Alzheimer's Disease Proteinopathy.International journal of molecular sciences · 2023Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
T lymphocytes are key contributors to the acute phase of cerebral ischemia reperfusion injury, but the relevant T cell-derived mediators of tissue injury remain unknown. Using a mouse model of transient focal brain ischemia, we report that IL-21 is highly up-regulated in the injured mouse brain after cerebral ischemia. IL-21-deficient mice have smaller infarcts, improved neurological function, and reduced lymphocyte accumulation in the brain within 24 h of reperfusion. Intracellular cytokine staining and adoptive transfer experiments revealed that brain-infiltrating CD4(+) T cells are the predominant IL-21 source. Mice treated with decoy IL-21 receptor Fc fusion protein are protected from reperfusion injury. In postmortem human brain tissue, IL-21 localized to perivascular CD4(+) T cells in the area surrounding acute stroke lesions, suggesting that IL-21-mediated brain injury may be relevant to human 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.