ArticleStroke and vascular neurology2023
Group 2 innate lymphoid cells resolve neuroinflammation following cerebral ischaemia.
Article in Stroke and vascular neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Pachymic Acid Promotes ILC2 Migration to the Brain via Dynein Axonemal Heavy Chain 9 Upregulation.Molecular neurobiology · 2025Article
- Choroid Plexus Fibroblast-ILC2 Niche Promotes Adult Hippocampal Neurogenesis after Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- IFP35, a novel DAMP, aggravates neuroinflammation following acute ischemic stroke via TLR4/NF-κB/NLRP3 signaling.Journal of neuroinflammation · 2025Article
- Cross-regulation between the nervous system and type 2 immunity.Science immunology · 2025Review
- Identification of novel inflammatory response-related biomarkers in patients with ischemic stroke based on WGCNA and machine learning.European journal of medical research · 2025Article
- Recent advances in research on common targets of neurological and sex hormonal influences on asthma.Clinical and translational allergy · 2025Review
- Expanding Role of Interleukin-1 Family Cytokines in Acute Ischemic Stroke.International journal of molecular sciences · 2024Review
- Microglia LILRB4 upregulation reduces brain damage after acute ischemic stroke by limiting CD8Journal of neuroinflammation · 2024Article
- Innate lymphoid cells in neuroinflammation.Frontiers in cellular neuroscience · 2024Review
- Current views on meningeal lymphatics and immunity in aging and Alzheimer's disease.Molecular neurodegeneration · 2023Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute brain ischaemia elicits pronounced inflammation, which aggravates neural injury. However, the mechanisms governing the resolution of acute neuroinflammation remain poorly understood. In contrast to regulatory T and B cells, group 2 innate lymphoid cells (ILC2s) are immunoregulatory cells that can be swiftly mobilised without antigen presentation; whether and how these ILC2s participate in central nervous system inflammation following brain ischaemia is still unknown.
methodsLeveraging brain tissues from patients who had an ischaemic stroke and a mouse model of focal ischaemia, we characterised the presence and cytokine release of brain-infiltrating ILC2s. The impact of ILC2s on neural injury was evaluated through antibody depletion and ILC2 adoptive transfer experiments. Using Rag2
resultsWe demonstrate that ILC2s accumulate in the areas surrounding the infarct in brain tissues of patients with cerebral ischaemia, as well as in mice subjected to focal cerebral ischaemia. Oligodendrocytes were a major source of IL-33, which contributed to ILC2s mobilisation. Adoptive transfer and expansion of ILC2s reduced brain infarction. Importantly, brain-infiltrating ILC2s reduced the magnitude of stroke injury severity through the production of IL-4.
conclusionsOur findings revealed that brain ischaemia mobilises ILC2s to curb neuroinflammation and brain injury, expanding the current understanding of inflammatory networks following stroke.
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