ArticleFrontiers in immunology2017
Elevated Levels of Proinflammatory Cytokines in Cerebrospinal Fluid of Multiple Sclerosis Patients.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 158 citations in OpenAlex.
- Elucidating the bidirectional association between autoimmune diseases and depression: a systematic review and meta-analysis.BMJ mental health · 2024Pooled it
- Effects of thoracic manipulation with trigger point therapy on inflammatory cytokine levels in individuals with multiple sclerosis: a pilot study.Frontiers in rehabilitation sciences · 2026Trial
- Long-Term Suppression of Circulating Proinflammatory Cytokines in Multiple Sclerosis Patients Following Autologous Haematopoietic Stem Cell Transplantation.Frontiers in immunology · 2021Trial
- Effect of intrathecal injection of mesenchymal stem cell-neural progenitors on cerebrospinal fluid biomarkers in progressive multiple sclerosis.Stem cells translational medicine · 2026Article
- Serum Levels of the Proinflammatory Cytokines IL-6, IL-16, IL-18, and IL-36 in Patients with Multiple Sclerosis from the Western Region of Saudi Arabia: Associations with Disease Duration and Disability.Neurology international · 2026Article
- Refined single-cell profiling captures a CCR5EBioMedicine · 2026Article
- Inflammatory Mediators of Alzheimer's Disease Characterized in a Mouse Model (APP/PS1).NeuroSci · 2026Article
- A novel multiplexed biomarker panel reveals key molecular pathways in progressive multiple sclerosis.Brain communications · 2026Article
- Multiple sclerosis and autoimmunity: a reappraisal of the evidence.Frontiers in immunology · 2026Review
- T Helper Cells and Cytokine Networks in the Immunopathogenesis of Multiple Sclerosis.ImmunoTargets and therapy · 2026Review
- Endothelial-to-mesenchymal transition in the central nervous system: A potential therapeutic target to combat age-related vascular fragility.The Journal of pharmacology and experimental therapeutics · 2025Review
- Multivariate analysis of glycogenes reveals coordinated regulation of immunoglobulin glycosylation in an immortalized human B cell system.bioRxiv : the preprint server for biology · 2025Article
- Systemic Inflammation at the Crossroad of Major Depressive Disorder and Comorbidities: A Narrative Review.International journal of molecular sciences · 2025Review
- Semaphorin-3A in autoimmune rheumatic diseases: immunological and pathological aspects.Inflammopharmacology · 2025Review
- MSC transplantation ameliorates depression in lupus by suppressing Th1 cell-shaped synaptic stripping.JCI insight · 2025Article
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Vitamin D Supplementation Mediates a Shift toward Anti-Inflammatory Cytokine Response in Multiple Sclerosis.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025Article
- New serum soluble factors predicting inflammatory and non-inflammatory disability worsening in multiple sclerosis.Frontiers in immunology · 2025Article
- T-cell repertoire correlates with cytokine imbalance in multiple sclerosis patients.Frontiers in immunology · 2025Article
- A role of CD20Frontiers in immunology · 2025Article
34 more citing papers are in PubMed but not listed here.
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 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is an autoimmune neurodegenerative disease characterized by chronic brain inflammation. Leukocyte infiltration of brain tissue causes inflammation, demyelination, and the subsequent formation of sclerotic plaques, which are a hallmark of MS. Activation of proinflammatory cytokines is essential for regulation of lymphocyte migration across the blood-brain barrier. We demonstrate increased levels of many cytokines, including IL-2RA, CCL5, CCL11, MIF, CXCL1, CXCL10, IFNγ, SCF, and TRAIL, were upregulated in cerebrospinal fluid (CSF), whereas IL-17, CCL2, CCL3, CCL4, and IL-12(p40) were activated in MS serum. Interaction analysis of cytokines in CSF demonstrated a connection between IFNγ and CCL5 as well as MIF. Many cells can contribute to production of these cytokines including CD8 and Th1 lymphocytes and astrocytes. Therefore, we suggest that IFNγ released by Th1 lymphocytes can activate astrocytes, which then produce chemoattractants, including CCL5 and MIF. These chemokines promote an inflammatory milieu and interact with multiple chemokines including CCL27 and CXCL1. Of special note, upregulation of CCL27 was found in CSF of MS cases. This observation is the first to demonstrate CCL27 as a potential contributor of brain pathology in MS. Our data suggest that CCL27 may be involved in activation and migration of autoreactive encephalitogenic immune effectors in the brain. Further, our data support the role of Th1 lymphocytes in the pathogenesis of brain inflammation in MS, with several cytokines playing a central role.
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What OpenQuestion holds
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.