ArticleCell death & disease2021
The immune-inflammatory response of oligodendrocytes in a murine model of preterm white matter injury: the role of TLR3 activation.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.
- Long-term neurodevelopment in preterm neonates with necrotizing enterocolitis: systematic review and meta-analysis.Frontiers in neuroscience · 2026Pooled it
- From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).Molecular medicine reports · 2026Review
- Glial Cysteine Cathepsins: From Homeostasis to Neurodegeneration.Cellular and molecular neurobiology · 2026Review
- Gintonin prevents paclitaxel-induced neuropathic pain via spinal LPAJournal of ginseng research · 2026Article
- Oligodendroglia as Active Immunomodulators in Demyelinating Diseases.Neuroscience bulletin · 2026Review
- The role of persistent inflammation in failed recovery after perinatal brain injury: is resolution the cure?Journal of neuroinflammation · 2026Review
- From Breath to Brain: NICU respiratory interventions and bedside brain signal entropy predict later autism risk.Developmental cognitive neuroscience · 2026Article
- The glia-immune network: Astrocytes and oligodendrocytes as microglial co-ordinators in health and disease.The Journal of physiology · 2026Review
- A systematic scoring system to optimise the testing of neurotherapeutics in models of perinatal brain injury, with an applied case study of human umbilical-cord MSC.Journal of neuroinflammation · 2025Article
- Mechanisms and Clinical Significance of Endosomal Toll-Like Receptors in Neurological Diseases.Molecular neurobiology · 2025Review
- Article
- Microglial activation is inhibited by selective anti-seizure medications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- The shifting landscape of the preterm brain.Neuron · 2025Review
- Single-cell transcriptome of mouse hippocampus identifies neural precursor-like cells, and reveals IL15Rα knock out-mediated neuron remodeling.BMC genomics · 2025Article
- Inflammation alters myeloid cell and oligodendroglial iron-handling in multiple sclerosis.Acta neuropathologica communications · 2025Article
- Mitochondrial Dysfunction is a Crucial Immune Checkpoint for Neuroinflammation and Neurodegeneration: mtDAMPs in Focus.Molecular neurobiology · 2025Review
- Oligodendrocyte-specific overexpression of human alpha-synuclein results in elevated MBP levels and inflammatory responses in TgM83 mice, mimicking the pathological features of multiple system atrophy.Acta neuropathologica communications · 2025Article
- Review
- Prenatal inflammation exacerbates hyperoxia-induced neonatal brain injury.Journal of neuroinflammation · 2025Article
- Neuroinflammatory Proteins in Huntington's Disease: Insights into Mechanisms, Diagnosis, and Therapeutic Implications.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A leading cause of preterm birth is the exposure to systemic inflammation (maternal/fetal infection), which leads to neuroinflammation and white matter injury (WMI). A wide range of cytokines and chemokines are expressed and upregulated in oligodendrocytes (OLs) in response to inflammation and numerous reports show that OLs express several receptors for immune related molecules, which enable them to sense inflammation and to react. However, the role of OL immune response in WMI is unclear. Here, we focus our study on toll-like receptor-3 (TLR3) that is activated by double-strand RNA (dsRNA) and promotes neuroinflammation. Despite its importance, its expression and role in OLs remain unclear. We used an in vivo mouse model, which mimics inflammation-mediated WMI of preterm born infants consisting of intraperitoneal injection of IL-1β from P1 to P5. In the IL-1β-treated animals, we observed the upregulation of Tlr3, IL-1β, IFN-β, Ccl2, and Cxcl10 in both PDGFRα+ and O4+ sorted cells. This upregulation was higher in O4+ immature OLs (immOLs) as compared to PDGFRα+ OL precursor cells (OPCs), suggesting a different sensitivity to neuroinflammation. These observations were confirmed in OL primary cultures: cells treated with TLR3 agonist Poly(I:C) during differentiation showed a stronger upregulation of Ccl2 and Cxcl10 compared to cells treated during proliferation and led to decreased expression of myelin genes. Finally, OLs were able to modulate microglia phenotype and function depending on their maturation state as assessed by qPCR using validated markers for immunomodulatory, proinflammatory, and anti-inflammatory phenotypes and by phagocytosis and morphological analysis. These results show that during inflammation the response of OLs can play an autonomous role in blocking their own differentiation: in addition, the immune activation of OLs may play an important role in shaping the response of microglia during inflammation.
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