ArticleFrontiers in cellular neuroscience2020
Antigen-Dependent T Cell Response to Neural Peptides After Human Ischemic Stroke.
Article in Frontiers in cellular neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Trial
- The kallikrein-kinin system modulates CD4Journal of neuroinflammation · 2026Article
- Stem Cells in Post-Stroke Regenerative Therapy: Current Role of Wharton's Jelly Mesenchymal Stem Cells in the Orchestrum.Brain sciences · 2026Review
- 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
- Stem cell-mediated recovery in stroke: partnering with the immune system.Nature reviews. Neuroscience · 2026Review
- 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
- Umbilical mesenchymal stem cells mitigate T-cell compartments shift and Th17/Treg imbalance in acute ischemic stroke via mitochondrial transfer.Stem cell research & therapy · 2025Article
- Long-Term Accumulation of T Cytotoxic 1, T Cytotoxic 17, and T Cytotoxic 17/1 Cells in the Brain Contributes to Microglia-Mediated Chronic Neuroinflammation After Ischemic Stroke.Neuromolecular medicine · 2024Article
- Novel subsets of peripheral immune cells associated with promoting stroke recovery in mice.CNS neuroscience & therapeutics · 2024Article
- Peripheral blood transcriptomic analysis identifies potential inflammation and immune signatures for central retinal artery occlusion.Scientific reports · 2024Article
- Perspective from single-cell sequencing: Is inflammation in acute ischemic stroke beneficial or detrimental?CNS neuroscience & therapeutics · 2024Review
- Assessment of corticospinal tract damage and cytokines response in early and late stages of acute unilateral brainstem infarction patients.Frontiers in immunology · 2024Article
- Thromboinflammatory challenges in stroke pathophysiology.Seminars in immunopathology · 2023Review
- Hyperacute immune responses associate with immediate neuropathology and motor dysfunction in large vessel occlusions.Annals of clinical and translational neurology · 2023Article
- Tumor Necrosis Factor (TNF)-α-Stimulated Gene 6 (TSG-6): A Promising Immunomodulatory Target in Acute Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Correlation Between Cognitive Impairment and Homocysteine and S100B Protein in Patients with Progressive Ischemic Stroke.Neuropsychiatric disease and treatment · 2023Article
- Novel insight into cGAS-STING pathway in ischemic stroke: from pre- to post-disease.Frontiers in immunology · 2023Review
- Cell Heterogeneity Uncovered by Single-Cell RNA Sequencing Offers Potential Therapeutic Targets for Ischemic Stroke.Aging and disease · 2022Review
- Revisiting regulatory T cells for stroke therapy.The Journal of clinical investigation · 2022Article
- Anti-Inflammatory Gene Therapy Improves Spatial Memory Performance in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemic stroke causes brain tissue damage and may release central nervous system (CNS)-specific peptides to the periphery. Neural antigen presentation in the lymphoid tissue could prime immune cells and result in adaptive immune response. However, autoimmune responses against neural antigens are not commonly uncovered after stroke. We studied the brain tissue of nine fatal stroke cases and the blood of a cohort of 13 patients and 11 controls. Flow cytometry carried out in three of the brain samples showed CD8 and CD4 T cells in the cerebrospinal fluid (CSF) of the ventricles in the patient deceased 1 day poststroke, T cells with an activated phenotype in the CSF of the patient that died at day 6, and T cells in the ischemic brain tissue in the patient deceased 140 days after stroke onset. Immunohistochemistry showed higher T cell numbers in the core of the lesion of the patient deceased 18 days post-stroke than in the patients deceased from 1 to 5 days post-stroke. In blood samples, we studied whether lymphocytes were primed in the periphery against neural antigens at sequential times (on admission, day 5, and day 90) after stroke. T lymphocytes of stroke patients produced IFN-γ and TNF-α and responded to MBP peptides by increasing their production of TNF-α and IL-10 at admission, but not at later time points. In contrast, IL-4 producing T cells showed progressive increases. Higher percentages of TNF-α producing T lymphocytes at admission were independently associated with poorer outcomes at 90 days. However, we did not detect T cell responses to neural-antigen stimulation 90 days post-stroke. Altogether the results suggest acute T cell priming in the periphery in acute stroke, T cell trafficking from the CSF to the ischemic brain tissue, and the existence of active mechanisms preventing autoreactivity.
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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.