ArticleBrain, behavior, and immunity2011
Endothelial IL-1R1 is a critical mediator of EAE pathogenesis.
Article in Brain, behavior, and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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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.
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Who cites it
40 citing papers in PubMed, 48 citations in OpenAlex.
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- CSF1R ligands promote microglial proliferation but are not the sole regulators of developmental microglial proliferation.Development (Cambridge, England) · 2025Article
- IL-1 protects from fatal systemic candidiasis in mice by inhibiting oxidative phosphorylation and hypoxia.Nature communications · 2025Article
- Macrophage-targeted PEGylated liposomes ameliorate experimental autoimmune encephalomyelitis.Frontiers in immunology · 2025Article
- Conditional Knockout of IL-1R1 in Endothelial Cells Attenuates Seizures and Neurodegeneration via Inhibiting Neuroinflammation Mediated by Nrf2/HO-1/NLRP3 Signaling in Status Epilepticus Model.Molecular neurobiology · 2024Article
- The Role of Neutrophils in Multiple Sclerosis and Ischemic Stroke.Brain sciences · 2024Review
- Schizophrenia in the genetic era: a review from development history, clinical features and genomic research approaches to insights of susceptibility genes.Metabolic brain disease · 2024Review
- Identification of novel biomarkers linking depressive disorder and Alzheimer's disease based on an integrative bioinformatics analysis.BMC genomic data · 2023Article
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- The alarmin interleukin-1α triggers secondary degeneration through reactive astrocytes and endothelium after spinal cord injury.Nature communications · 2022Article
- The Therapeutic Prospects of Targeting IL-1R1 for the Modulation of Neuroinflammation in Central Nervous System Disorders.International journal of molecular sciences · 2022Review
- Cytokines in the Brain and Neuroinflammation: We Didn't Starve the Fire!Pharmaceuticals (Basel, Switzerland) · 2022Review
- Astrocytic YAP protects the optic nerve and retina in an experimental autoimmune encephalomyelitis model through TGF-β signaling.Theranostics · 2021Article
- Blocking PDGF-CC signaling ameliorates multiple sclerosis-like neuroinflammation by inhibiting disruption of the blood-brain barrier.Scientific reports · 2020Article
- Interleukin-1 promotes autoimmune neuroinflammation by suppressing endothelial heme oxygenase-1 at the blood-brain barrier.Acta neuropathologica · 2020Article
- Neuronal interleukin-1 receptors mediate pain in chronic inflammatory diseases.The Journal of experimental medicine · 2020Article
- Neutrophils: Underestimated Players in the Pathogenesis of Multiple Sclerosis (MS).International journal of molecular sciences · 2020Review
- Neutrophil-selective deletion of Cxcr2 protects against CNS neurodegeneration in a mouse model of multiple sclerosis.Journal of neuroinflammation · 2020Article
- Interleukin-1 mediates ischaemic brain injury via distinct actions on endothelial cells and cholinergic neurons.Brain, behavior, and immunity · 2019Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Interleukin-1 (IL-1) has been implicated in the disease progression of multiple sclerosis (MS). In the animal model of MS, experimental autoimmune encephalomyelitis (EAE), the induction of disease is significantly attenuated in mice lacking the type I IL-1 receptor (IL-1R1). In this study, we created a transgenic mouse (eIL-1R1 kd) in which IL-1R1 expression is knocked down specifically in endothelial cells. Induction of EAE in eIL-1R1 kd mice results in a decrease in incidence, severity and delayed onset of EAE. In addition, eIL-1R1 kd mice show significant decrease in VCAM-1 expression and diminished CD45(+) and CD3(+) infiltrating leukocytes in the spinal cord in animals challenged with EAE. Further, IL-1 and IL-23 stimulate IL-17 production by splenocytes from both wild type and the eIL-1R1 kd animals. Similarly, IL-1 and IL-23 synergistically stimulate splenocytes proliferation in these two strains of animals. After immunization with MOG(79-96), although eIL-1R1 kd mice displayed greatly reduced clinical scores, their splenocytes produced IL-17 and proliferated in response to a second MOG challenge, similar to wild type animals. These findings indicate a critical role for endothelial IL-1R1 in mediating the pathogenesis of EAE, and describe a new model that can be used to study endothelial IL-1R1.
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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.