ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Antigen dependently activated cluster of differentiation 8-positive T cells cause perforin-mediated neurotoxicity in experimental stroke.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 114 citations in OpenAlex.
- Integrated B and T Cell Repertoire Analysis Reveals Organized but Heterogeneous Adaptive Immunity in Chronic Experimental Stroke.Research square · 2026Article
- Microbiota, systemic immunity, and extracellular vesicles in stroke: peripheral nodes as therapeutic leverage points.Journal of neuroinflammation · 2026Review
- Targeting T cell metabolism and polarization to modulate post-stroke immune responses and improve outcomes.Frontiers in immunology · 2026Article
- Lack of Negative Feedback Loops of CTLA-4 and PD-L1 as Key Mechanisms for Post-Acute T Cell Activation Until 3 Months After Ischemic Stroke.International journal of molecular sciences · 2025Article
- Natural killer cell-derived granzyme B as a therapeutic target for alleviating graft injury during liver transplantation.Acta pharmaceutica Sinica. B · 2025Article
- Comprehensive insight on immune landscape in intracerebral hemorrhage patients with single-cell RNA sequencing: from blood to hematoma.Journal of neuroinflammation · 2025Article
- Semaglultide targets Spp1Journal of neuroinflammation · 2025Article
- Diagnostic biomarkers and immune infiltration profiles common to COVID-19, acute myocardial infarction and acute ischaemic stroke using bioinformatics methods and machine learning.BMC neurology · 2025Article
- The Aging Immune System: A Critical Attack on Ischemic Stroke.Molecular neurobiology · 2025Review
- Skull bone marrow and skull meninges channels: redefining the landscape of central nervous system immune surveillance.Cell death & disease · 2025Review
- CD8 cell-derived granzyme B may be a predictor for coronary artery involvement and MACE in Takayasu arteritis patients.Clinical and experimental immunology · 2025Article
- Immune-mediated blood-brain barrier disruption after ischemic stroke: mechanisms and therapeutic targets.Frontiers in immunology · 2025Review
- Neuroinflammation and acute ischemic stroke: impact on translational research and clinical care.Frontiers in surgery · 2025Review
- Circulating CD4+, CD8+, and double-negative T cells in ischemic stroke and stroke-associated infection: a prospective case-control study.Frontiers in cellular neuroscience · 2025Article
- Chuanxiong Rhizoma regulates ferroptosis and the immune microenvironment in ischemic stroke through the JAK-STAT3 pathway.Scientific reports · 2024Article
- Perioperative stroke deteriorates white matter integrity by enhancing cytotoxic CD8CNS neuroscience & therapeutics · 2024Article
- The Involvement of Immune Cells Between Ischemic Stroke and Gut Microbiota.Translational stroke research · 2024Review
- Inflammatory response in traumatic brain and spinal cord injury: The role of XCL1-XCR1 axis and T cells.CNS neuroscience & therapeutics · 2024Review
- Age-Related Alterations in Immune Function and Inflammation: Focus on Ischemic Stroke.Aging and disease · 2024Review
- Novel subsets of peripheral immune cells associated with promoting stroke recovery in mice.CNS neuroscience & therapeutics · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation plays a key role in secondary brain damage after stroke. Although deleterious effects of proinflammatory cytokines are well characterized, direct cytotoxic effects of invading immune cells on the ischemic brain and the importance of their antigen-dependent activation are essentially unknown. Here we examined the effects of adaptive and innate immune cells-cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells-that share the direct perforin-mediated cytotoxic pathway on outcome after cerebral ischemia in mice. Although CTLs and NK cells both invaded the ischemic brain, only brain-infiltrating CTLs but not NK cells were more activated than their splenic counterparts. Depletion of CTLs decreased infarct volumes and behavioral deficit in two ischemia models, whereas NK cell depletion had no effect. Correspondingly, adoptive CTL transfer from wild-type into Rag1 knock-out mice increased infarct size. Adoptive CTL transfer from perforin knock-out or interferon-γ knock-out mice into Rag1 knock-out mice revealed that CTL neurotoxicity was mediated by perforin. Accordingly, CTLs isolated from wild-type or interferon-γ knock-out but not from perforin knock-out mice induced neuronal cell death in vitro. CTLs derived from ovalbumin-specific T-cell receptor transgenic mice were not activated and infiltrated less into the ischemic brain compared with wild-type CTLs. Their transfer did not increase the infarct size of Rag1 knock-out mice, indicating antigen-dependent activation as an essential component of CTL neurotoxicity. Our findings underscore the importance of antigen-dependent, direct cytotoxic immune responses in stroke and suggest modulation of CTLs and their effector pathways as a potential new strategy for stroke therapy.
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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.