ArticleFrontiers in neurology2017
IL-2/Anti-IL-2 Complex Attenuates Inflammation and BBB Disruption in Mice Subjected to Traumatic Brain Injury.
Article in Frontiers in neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Traumatic MicroRNAs: Deconvolving the Signal After Severe Traumatic Brain Injury.Cellular and molecular neurobiology · 2023Pooled it
- Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.Molecular neurobiology · 2026Review
- Cytokines and related signaling pathways in traumatic brain injury.Frontiers in immunology · 2026Review
- Differences in inflammatory markers, mitochondrial function, and synaptic proteins in male and female Alzheimer's disease post mortem brains.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- T Cell Involvement in Neuroinflammation After Traumatic Brain Injury: Implications for Therapeutic Intervention.CNS neuroscience & therapeutics · 2025Review
- Breaking the Barrier: The Role of Proinflammatory Cytokines in BBB Dysfunction.International journal of molecular sciences · 2025Review
- Nasal anti-CD3 monoclonal antibody ameliorates traumatic brain injury, enhances microglial phagocytosis and reduces neuroinflammation via IL-10-dependent TNature neuroscience · 2025Article
- Serum cytokine profiles at near term-equivalent age and their association with neurodevelopmental outcomes in preterm infants: an exploratory study.Frontiers in pediatrics · 2025Article
- Cerebrospinal fluid markers of neuroinflammation and coagulation in severe cerebral edema and chronic hydrocephalus after subarachnoid hemorrhage: a prospective study.Journal of neuroinflammation · 2024Article
- Low-Dose Interleukin-2 Reverses Traumatic Brain Injury-Induced Cognitive Deficit and Pain in a Murine Model.Annals of neurology · 2024Article
- The path to next-generation disease-modifying immunomodulatory combination therapies in Alzheimer's disease.Nature aging · 2024Review
- Regulatory T lymphocytes in traumatic brain injury.Neurochemistry international · 2024Review
- Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer's models.Cell reports · 2022Article
- Article
- Crossing nerve transfer drives sensory input-dependent plasticity for motor recovery after brain injury.Science advances · 2022Article
- Brain-Derived Extracellular Vesicles Induce Vasoconstriction and Reduce Cerebral Blood Flow in Mice.Journal of neurotrauma · 2022Article
- The Obese Brain: Mechanisms of Systemic and Local Inflammation, and Interventions to Reverse the Cognitive Deficit.Frontiers in integrative neuroscience · 2022Review
- Regulatory T cells protect against brain damage by alleviating inflammatory response in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2021Article
- A new inflammatory parameter can predict delayed intracranial hemorrhage following ventriculoperitoneal shunt.Scientific reports · 2021Article
- Involvement of mTOR Pathways in Recovery from Spinal Cord Injury by Modulation of Autophagy and Immune Response.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Traumatic brain injury (TBI) induces the excessive inflammation and disruption of blood-brain barrier, both of which are partially mediated by the activation of microglia and release of inflammatory cytokines. Previous reports showed that administration of regulatory T cells (Tregs) could suppress inflammation and promote neurological function recovery, and that the IL-2/anti-IL-2 complex (IL-2C) could increase the number of Tregs. Thus, we hypothesized that IL-2C-mediated expansion of Tregs would be beneficial in mice subjected to TBI. In this study, mice received an intraperitoneal injection of IL-2C for three consecutive days. We observed that IL-2C dose-dependently increased Tregs without affecting the populations of CD4, CD8, or natural killer cells. IL-2C could improve the neurological recovery and reduce brain edema, tissue loss, neutrophils infiltration, and tight junction proteins degradation. Furthermore, this complex could also reduce the expression of CD16/32, IL-1β, or TNF-α, and elevate the expression of CD206, arginase 1, or TGF-β. These results suggest that IL-2C could be a potential therapeutic method to alleviate excessive inflammation and maintain blood vessel stability after TBI.
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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.