ArticleNeuromolecular medicine2021
IL-2/IL-2R Antibody Complex Enhances Treg-Induced Neuroprotection by Dampening TNF-α Inflammation in an In Vitro Stroke Model.
Article in Neuromolecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Harnessing Regulatory T Cells to Modulate Acute Brain Injury: From Mechanisms to Therapy.Molecular neurobiology · 2026Review
- Placental and juvenile immune responses to maternal immune activation are differentially regulated by sex chromosomes and gonads across gestation.Journal of neuroinflammation · 2026Article
- Regulatory T cells in stroke inflammation: Therapeutic perspectives.Neural regeneration research · 2026Article
- Evaluation of the anti-apoptotic, anti-platelet aggregation, and pro-angiogenic properties of Naoshuantong capsule in ischemic stroke: insights from network pharmacology and animal experiments.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- IL-2: a promising topical treatment for Sjögren's disease-related dry eye disease.Arthritis research & therapy · 2026Article
- Article
- Neuroinflammation and acute ischemic stroke: impact on translational research and clinical care.Frontiers in surgery · 2025Review
- Getting the guts to expand stroke treatment: The potential for microbiome targeted therapies.CNS neuroscience & therapeutics · 2023Review
- Regulatory T lymphocytes as a therapy for ischemic stroke.Seminars in immunopathology · 2023Review
- Autoimmune Neuroinflammatory Diseases: Role of Interleukins.International journal of molecular sciences · 2023Review
- Tumor Necrosis Factor-Disease markers · 2022Review
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present in vitro study showed that IL-2/IL-2R antibody complex facilitates Treg-induced neuroprotection in the oxygen glucose deprivation/reoxygenation (OGD/R) model of stroke. First, we examined the role of IL-2/IL-2R-treated Tregs in OGD/R-exposed rat primary cortical cells (PCCs), which represent the cell type of the ischemic gray matter in the stroke brain. Here, OGD/R induced cell death, which was attenuated by Tregs and more robustly by IL-2/IL-2R-treated Tregs, but not by IL-2/IL-2R treatment alone. Second, we next assessed IL-2/IL-2R effects in OGD/R-exposed human oligodendrocyte progenitor cells (OPCs), which correspond to the white matter injury after stroke. Results revealed that a similar pattern neuroprotection as seen in the gray matter, in that OGD/R triggered cell death, which was ameliorated by Tregs and more effectively by IL-2/IL-2R-treated Tregs, but IL-2/IL-2R treatment alone was not therapeutic. Third, as we begin to understand the mechanism underlying IL-2/IL-2R engagement of Tregs, we investigated the inflammatory response in OGD/R-exposed human neural progenitor cells (NPCs), which recapitulate both ischemic gray and white matter damage in stroke. Similar to PCCs and OPCs, OGD/R produced cell death and was blocked by Tregs and more efficiently by IL-2/IL-2R-treated Tregs, whereas IL-2/IL-2R treatment alone did not alter the ischemic insult. Moreover, the inflammatory marker, TNF-α, was upregulated after OGD/R, dampened by both Tregs and more efficiently by IL-2/IL-2R-treated Tregs but more pronounced in the latter, and not affected by IL-2/IL-2R treatment alone, suggesting IL-2/IL-2R-Treg-mediated modulation of inflammatory response in stroke. Altogether, these observations support the use of IL-2/IL-2R treatment in enhancing the anti-inflammatory effects of Tregs in stroke.
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