ArticleThe Journal of experimental medicine2021
Chronic T cell proliferation in brains after stroke could interfere with the efficacy of immunotherapies.
Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The trial behind it
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Who cites it
32 citing papers in PubMed.
- Isolation and identification of leukocyte populations in intracranial blood collected during mechanical thrombectomy.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Trial
- Infarct-associated oligoclonal T cell expansion in chronic experimental stroke across age, sex, and models.Experimental neurology · 2026Article
- The kallikrein-kinin system modulates CD4Journal of neuroinflammation · 2026Article
- Immune-mediated excitotoxicity in brain disorders.Nature reviews. Immunology · 2026Review
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Neuroinflammation in Ischemic Stroke: Mechanisms, Systemic Interactions, and Therapeutic Targets.Translational stroke research · 2026Review
- "The emerging role of lymphocytes in post-stroke inflammation: A treatable target and review of current pharmacological evidence in humans".Brain, behavior, & immunity - health · 2026Review
- Spatiotemporally precise immune reprogramming: a new paradigm for next-generation neuroimmune therapy in ischemic stroke.Frontiers in neurology · 2026Review
- Harnessing extracellular vesicles for ischemic stroke management.Regenerative biomaterials · 2026Review
- Peripheral CD200R signaling: A critical regulator of post-stroke inflammation in aged mice.Brain research bulletin · 2026Article
- Article
- Nanoparticle-Mediated Nose-to-Brain Delivery for Ischemic Stroke Therapy: Preclinical Insights.Pharmaceutics · 2025Review
- Changes in Neuroimmunological Synapses During Cerebral Ischemia.Translational stroke research · 2025Review
- HMGB1: A New Target for Ischemic Stroke and Hemorrhagic Transformation.Translational stroke research · 2025Review
- Neural repair mechanisms after ischemic stroke.Inflammation and regeneration · 2025Review
- The immunology of stroke and dementia.Immunity · 2025Review
- CD4Frontiers in immunology · 2025Review
- Anti-CD49d Ab treatment ameliorates age-associated inflammatory response and mitigates CD8Journal of neuroinflammation · 2024Article
- Regional desynchronization of microglial activity is associated with cognitive decline in Alzheimer's disease.Molecular neurodegeneration · 2024Article
- Age-Related Alterations in Immune Function and Inflammation: Focus on Ischemic Stroke.Aging and disease · 2024Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Neuroinflammation is an emerging focus of translational stroke research. Preclinical studies have demonstrated a critical role for brain-invading lymphocytes in post-stroke pathophysiology. Reducing cerebral lymphocyte invasion by anti-CD49d antibodies consistently improves outcome in the acute phase after experimental stroke models. However, clinical trials testing this approach failed to show efficacy in stroke patients for the chronic outcome 3 mo after stroke. Here, we identify a potential mechanistic reason for this phenomenon by detecting chronic T cell accumulation-evading the systemic therapy-in the post-ischemic brain. We observed a persistent accumulation of T cells in mice and human autopsy samples for more than 1 mo after stroke. Cerebral T cell accumulation in the post-ischemic brain was driven by increased local T cell proliferation rather than by T cell invasion. This observation urges re-evaluation of current immunotherapeutic approaches, which target circulating lymphocytes for promoting recovery after 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.