ArticleTranslational stroke research2012
A novel hypothesis: regulatory B lymphocytes shape outcome from experimental stroke.
Article in Translational stroke research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
42 citing papers in PubMed.
- CD19Frontiers in immunology · 2025Article
- The Role of Gut Microbiota in Blood-Brain Barrier Disruption after Stroke.Molecular neurobiology · 2024Review
- Mechanisms of inflammation after ischemic stroke in brain-peripheral crosstalk.Frontiers in molecular neuroscience · 2024Review
- Updates of the role of B-cells in ischemic stroke.Frontiers in cellular neuroscience · 2024Review
- Uncovering the dual roles of peripheral immune cells and their connections to brain cells in stroke and post-stroke stages through single-cell sequencing.Frontiers in neuroscience · 2024Review
- Inhibiting leukocyte-endothelial cell interactions by Chinese medicine Tongxinluo capsule alleviates no-reflow after arterial recanalization in ischemic stroke.CNS neuroscience & therapeutics · 2023Article
- Bystanders or not? Microglia and lymphocytes in aging and stroke.Neural regeneration research · 2023Review
- Subarachnoid hemorrhage triggers neuroinflammation of the entire cerebral cortex, leading to neuronal cell death.Inflammation and regeneration · 2022Article
- Roles of peripheral immune cells in the recovery of neurological function after ischemic stroke.Frontiers in cellular neuroscience · 2022Review
- Inflammation Mediated Epileptogenesis as Possible Mechanism Underlying Ischemic Post-stroke Epilepsy.Frontiers in aging neuroscience · 2021Review
- Comprehensive Landscape of Immune Infiltration and Aberrant Pathway Activation in Ischemic Stroke.Frontiers in immunology · 2021Article
- Adaptive Immunity Regulation and Cerebral Ischemia.Frontiers in immunology · 2020Review
- Histopathological features of oral lichen planus and its response to corticosteroid therapy: A retrospective study.Medicine · 2019Article
- Glucocorticoids Regulate Bone Marrow B Lymphopoiesis After Stroke.Circulation research · 2019Article
- Increased Peripheral CD137 Expression in a Mouse Model of Permanent Focal Cerebral Ischemia.Cellular and molecular neurobiology · 2019Article
- Transplantation of Lymphocytes Co-Cultured with Human Cord Blood-Derived Multipotent Stem Cells Attenuates Inflammasome Activity in Ischemic Stroke.Clinical interventions in aging · 2019Article
- Immunoreactive Cells After Cerebral Ischemia.Frontiers in immunology · 2019Review
- A review of the role of cav-1 in neuropathology and neural recovery after ischemic stroke.Journal of neuroinflammation · 2018Review
- Early Inflammatory Response in the Brain and Anesthesia Recovery Time Evaluation After Experimental Subarachnoid Hemorrhage.Translational stroke research · 2018Article
- Splenectomy Fails to Provide Long-Term Protection Against Ischemic Stroke.Aging and disease · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Although inflammatory immune cells clearly contribute to the development of middle cerebral artery occlusion (MCAO) in mice, the failure to block neutrophil-associated injury in clinical stroke trials has discouraged further development of immunotherapeutic approaches. However, there is renewed interest in a possible protective role for regulatory T- and B-cells that can suppress inflammation and limit central nervous system damage induced by infiltrating pro-inflammatory cells. Our failure to implicate CD4(+)FoxP3(+) T-cells in limiting brain lesion volume after MCAO turned our focus towards regulatory B-cells known to mediate protection against other inflammatory CNS conditions. Our results clearly demonstrated that B-cell deficient mice developed larger infarct volumes, higher mortality and more severe functional deficits compared to wild-type mice, and had increased numbers of activated T-cells, macrophages, microglial cells, and neutrophils in the affected brain hemisphere. These MCAO-induced changes were completely prevented in B-cell-restored mice after transfer of highly purified WT B-cells but not IL-10-deficient B-cells. Our novel observations are the first to implicate IL-10-secreting B-cells as a major regulatory cell type in stroke and suggest that enhancement of regulatory B-cells might have application as a novel therapy for this devastating neurologic condition.
Identifiers
What OpenQuestion holds
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.