ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2023
Inflammatory Cytokines Associated with Multiple Sclerosis Directly Induce Alterations of Neuronal Cytoarchitecture in Human Neurons.
Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.
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
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- Association between FDG- and TSPO-PET signals across human and animal studies investigating neurodegenerative conditions: a systematic review.Molecular psychiatry · 2026Pooled it
- Current Knowledge about Nonclassical Monocytes in Patients with Multiple Sclerosis, a Systematic Review.International journal of molecular sciences · 2024Pooled it
- The theory of the inflammatory ecosystem.Science China. Life sciences · 2026Review
- Short-Chain Fatty Acids at the Crossroads of Microbiota, Immunometabolism, and Inflammation.Biomedicines · 2026Review
- The Developmental and Functional Implications of Age-Associated B Cells (ABCs) Across Tissue Microenvironments.Immunological reviews · 2026Review
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- LncRNA AFAP1-AS1 mediates therapy-dependent expression of CCL5, CXCL10 and MMP9 in multiple sclerosis.Biochemistry and biophysics reports · 2026Article
- Association between cognitive dysfunction and upper extremity performance in multiple sclerosis: a cross-sectional study.Irish journal of medical science · 2026Article
- Article
- T Helper Cells and Cytokine Networks in the Immunopathogenesis of Multiple Sclerosis.ImmunoTargets and therapy · 2026Review
- Neurovascular dysfunction in the development and progression of neuroinflammatory diseases.Frontiers in cellular neuroscience · 2026Review
- Review
- Review
- FABP7 is increased in progressive multiple sclerosis and induces a pro-inflammatory phenotype in monocytes through a glycolytic switch.Nature communications · 2025Article
- Breaking the Cycle: Can Vitamin D Bridge the Gap Between Gut Microbiota and Immune Dynamics in Multiple Sclerosis?International journal of molecular sciences · 2025Review
- Cytokine Gene Expression and Treatment Impact on MRI Outcomes in Jordanian Patients with Multiple Sclerosis.Life (Basel, Switzerland) · 2025Article
- Identification of novel biomarkers associated with immune infiltration in major depression disorder and atopic dermatitis.Archives of dermatological research · 2025Article
- Predicting multiple sclerosis prognosis using AI and machine learning: integrating clinical, immunological, and radiological variables.Frontiers in neurology · 2025Article
- Fenebrutinib, a Bruton's tyrosine kinase inhibitor, blocks distinct human microglial signaling pathways.Journal of neuroinflammation · 2024Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) coined by inflammation and neurodegeneration. The actual cause of the neurodegenerative component of the disease is however unclear. We investigated here the direct and differential effects of inflammatory mediators on human neurons. We used embryonic stem cell-derived (H9) human neuronal stem cells (hNSC) to generate neuronal cultures. Neurons were subsequently treated with tumour necrosis factor alpha (TNFα), interferon gamma (IFNγ), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 17A (IL-17A) and interleukin 10 (IL-10) separately or in combination. Immunofluorescence staining and quantitative polymerase chain reaction (qPCR) were used to assess cytokine receptor expression, cell integrity and transcriptomic changes upon treatment. H9-hNSC-derived neurons expressed cytokine receptors for IFNγ, TNFα, IL-10 and IL-17A. Neuronal exposure to these cytokines resulted in differential effects on neurite integrity parameters with a clear decrease for TNFα- and GM-CSF-treated neurons. The combinatorial treatment with IL-17A/IFNγ or IL-17A/TNFα induced a more pronounced effect on neurite integrity. Furthermore, combinatorial treatments with two cytokines induced several key signalling pathways, i.e. NFκB-, hedgehog and oxidative stress signalling, stronger than any of the cytokines alone. This work supports the idea of immune-neuronal crosstalk and the need to focus on the potential role of inflammatory cytokines on neuronal cytoarchitecture and function.
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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.