ArticleJournal of neuroinflammation2025
Single-cell sequencing reveals intracranial microvasculature-derived CXCL12 promotes CD8
Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Remote Ischemic Post-Conditioning Preserves the Neurovascular Unit by Brain-Derived Gas6 That Drives Monocyte-Derived Macrophage Reprogramming via Axl and Vimentin after SAH.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Nanomedicine targeting neuroinflammatory pathways in Alzheimer's disease: a new frontier in inflammopharmacology.Inflammopharmacology · 2026Review
- Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.Molecular neurobiology · 2026Review
- Remote Ischemic Postconditioning Attenuates Neuroinflammation and Suggests a Potential Benefit for Early Neurological Recovery after Subarachnoid Hemorrhage via the IL-9/JAK2-STAT5 Signaling Pathway.Translational stroke research · 2026Article
- Microglia Attenuate Neuroinflammation After Subarachnoid Hemorrhage by Modulating Astrocyte Phenotypic Transformation via the RARα/Mafb/Msr1 Pathway.Molecular neurobiology · 2026Article
- Olink Proteomics Reveals CCL2 Aggravates Perihematomal Edema After Intracerebral Hemorrhage in High-Altitude Migrants Via CCR2/NF-κB-Mediated Blood-Brain Barrier Disruption.CNS neuroscience & therapeutics · 2026Article
- Amplitude-integrated electroencephalography for early diagnosis and severity assessment of neonatal intracranial hemorrhage: a multicenter retrospective study.Italian journal of pediatrics · 2026Article
- Beyond the Glial Scar: Fibroblasts as Dynamic Coordinators of Neuroprotection and Neuroinflammation Post-Brain Injury.Neuroscience bulletin · 2026Article
- Gut microbiota and metabolites as potential modulators of cognitive impairment after aneurysmal subarachnoid hemorrhage: a hypothesis-driven review.Frontiers in microbiology · 2026Review
- The immune-endothelial axis in neurovascular pathophysiology: a framework for targeted interventions.Frontiers in immunology · 2026Review
- Brain-cervical lymph node crosstalk contributes to brain injury induced by subarachnoid hemorrhage in mice.Nature communications · 2025Article
- Neuroimmune crosstalk in Parkinson's disease: the pivotal role of microglia and infiltrating T cells.Molecular biology reports · 2025Review
- T Cell Involvement in Neuroinflammation After Traumatic Brain Injury: Implications for Therapeutic Intervention.CNS neuroscience & therapeutics · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
backgroundProcesses related to how the intracranial microvasculature initiates brain‒peripheral crosstalk for subsequent blood‒brain barrier (BBB) dysfunction at an early stage after subarachnoid hemorrhage (SAH) ictus are still unknown. This study elucidated the effect and potential mechanism of intracranial microvasculature-mediated T-cell infiltration on BBB function after SAH.
methodsPublicly available single-cell RNA sequencing data related to SAH ( https://ngdc.cncb.ac.cn/omix ; Accession No. OMIX006611) were retrieved and analyzed. The dataset was derived from the white matter region of adult male C57BL/6J mice at 1 and 7 days after experimental SAH. The SAH model was induced by endovascular perforation, and experiments were subsequently conducted at 1, 3, 7, and 14 days after SAH to evaluate T-cell infiltration, BBB integrity, neuronal injury, and neurological function.
resultsAfter SAH, CXCL12 expression was increased in endothelial cells and pericytes, promoting CD8
conclusionThis study suggests that, following SAH, both pericytes and endothelial cells may contribute to immune regulation by producing CXCL12, which promotes CD8⁺ T-cell infiltration into the brain. This mechanism may play a role in BBB disruption and neurological dysfunction. Targeting the CXCL12-CXCR4 axis could offer a potential approach for mitigating immune-mediated injury after SAH.
Indexed as
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.