ArticleJCI insight2021
AMPK induces regulatory innate lymphoid cells after traumatic brain injury.
Article in JCI insight, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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.
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Who cites it
28 citing papers in PubMed, 46 citations in OpenAlex.
- Targeting IL-33 in Precision Neuroimmunology: Cellular Mechanisms and Therapeutic Strategies for CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Review
- Metformin as an Innate Immune Modulator: Metabolic and Epigenetic Reprogramming of Innate Immune Cells and Therapeutic Implications.Current issues in molecular biology · 2026Review
- Innate lymphoid cells: unsung heroes or villains in multiple sclerosis pathogenesis?Immunologic research · 2026Review
- IL-25-ILC2-IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity.Journal of neuroinflammation · 2026Article
- Adoptive transfer of ILC2s reveals tumor homing in glioblastoma: a proof-of-concept study.Frontiers in oncology · 2026Article
- Choroid Plexus Fibroblast-ILC2 Niche Promotes Adult Hippocampal Neurogenesis after Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Time of day dependent reduction in stroke infarct volume by the Reverb agonist SR9009 in mice.Experimental neurology · 2025Article
- Immune conversations at the border: meningeal immunity in health and disease.Frontiers in immunology · 2025Review
- Innate lymphoid cells in the spotlight: from biomarkers to blueprint for innovative immunotherapy.Frontiers in immunology · 2025Review
- High-temperature requirement serine protease A2 inhibitor UCF-101 ameliorates damaged neurons in traumatic brain-injured rats by the AMPK/NF-κB pathway.Open life sciences · 2025Article
- J147 treatment protects against traumatic brain injury by inhibiting neuronal endoplasmic reticulum stress potentially via the AMPK/SREBP-1 pathway.Translational research : the journal of laboratory and clinical medicine · 2024Article
- Metabolic-driven analytics of traumatic brain injury and neuroprotection by ethyl pyruvate.Journal of neuroinflammation · 2024Article
- Boosting Acetylcholine Signaling by Cannabidiol in a Murine Model of Alzheimer's Disease.International journal of molecular sciences · 2024Article
- The contribution of the meningeal immune interface to neuroinflammation in traumatic brain injury.Journal of neuroinflammation · 2024Review
- ICAM-1 Deletion Using CRISPR/Cas9 Protects the Brain from Traumatic Brain Injury-Induced Inflammatory Leukocyte Adhesion and Transmigration Cascades by Attenuating the Paxillin/FAK-Dependent Rho GTPase Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Group 2 innate lymphoid cells suppress neuroinflammation and brain injury following intracerebral hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Article
- Innate lymphoid cells in neuroinflammation.Frontiers in cellular neuroscience · 2024Review
- Review
- Inhalant Cannabidiol Inhibits Glioblastoma Progression Through Regulation of Tumor Microenvironment.Cannabis and cannabinoid research · 2023Article
- The role of innate lymphocytes in regulating brain and cognitive function.Neurobiology of disease · 2023Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
The CNS is regarded as an immunoprivileged organ, evading routine immune surveillance; however, the coordinated development of immune responses profoundly influences outcomes after brain injury. Innate lymphoid cells (ILCs) are cytokine-producing cells that are critical for the initiation, modulation, and resolution of inflammation, but the functional relevance and mechanistic regulation of ILCs are unexplored after acute brain injury. We demonstrate increased proliferation of all ILC subtypes within the meninges for up to 1 year after experimental traumatic brain injury (TBI) while ILCs were present within resected dura and elevated within cerebrospinal fluid (CSF) of moderate-to-severe TBI patients. In line with energetic derangements after TBI, inhibition of the metabolic regulator, AMPK, increased meningeal ILC expansion, whereas AMPK activation suppressed proinflammatory ILC1/ILC3 and increased the frequency of IL-10-expressing ILC2 after TBI. Moreover, intracisternal administration of IL-33 activated AMPK, expanded ILC2, and suppressed ILC1 and ILC3 within the meninges of WT and Rag1-/- mice, but not Rag1-/- IL2rg-/- mice. Taken together, we identify AMPK as a brake on the expansion of proinflammatory, CNS-resident ILCs after brain injury. These findings establish a mechanistic framework whereby immunometabolic modulation of ILCs may direct the specificity, timing, and magnitude of cerebral immunity.
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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.