ReviewCells2020
Re-Examining the Role of TNF in MS Pathogenesis and Therapy.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
79 citing papers in PubMed, 103 citations in OpenAlex.
- Autologous Hematopoietic Transplantation Reduces Brain Inflammatory and Axoglial Damage Biomarkers in Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2026Trial
- The Neuroimmune Duality of CD4⁺ T Cells: Drivers of Damage and Repair in the Brain.Molecular neurobiology · 2026Review
- Therapeutic evaluation of artocarpin-enriched extract from Artocarpus heterophyllus heartwood in multiple sclerosis rat model.Inflammopharmacology · 2026Article
- Therapeutic Effects of Combined 6-Shogaol and Ibudilast on Neuroinflammation and Behavioral Deficits in a Cuprizone Mouse Model of Multiple Sclerosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Article
- Anti-Neuroinflammatory Cannabinoid Acids as a New Therapeutic Approach for Multiple Sclerosis.Molecules (Basel, Switzerland) · 2026Article
- NEMO/IKKγ: Emerging player in the NF-κB pathway and potential therapeutic target in inflammation.Inflammation · 2026Review
- The effect of cladribine tablets on intrathecal inflammation in relapsing-remitting multiple sclerosis.Journal of neuroinflammation · 2026Article
- Glial Cells as Key Mediators in the Pathophysiology of Neurodegenerative Diseases.International journal of molecular sciences · 2026Review
- Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Review
- Cytokine Modulation and Antioxidant Defense Restoration by Jateorhiza macrantha (Menispermaceae) Leaf Extracts Mitigate CFA-Induced Hypernociception, Inflammation, and Pyrexia in Rats.BioMed research international · 2026Article
- Gut Microbiota-Derived Metabolites Regulate CASP3 and Neuroimmune Pathways in Multiple Sclerosis: An Integrative Multiomics Study.Mediators of inflammation · 2026Article
- The importance of TNF-α signaling: a potential risk factor in neurodegenerative and cardiovascular diseases.Archives of medical science : AMS · 2026Article
- IL-1β contributes to neurological disability in NMOSD AQP4 + Patients.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Article
- TNF as a mediator of metabolic inflammation and body-brain interaction in obesity-driven neuroinflammation and neurodegeneration.Ageing research reviews · 2025Review
- Article
- Restoration of the peace in autoimmune disease: tired of fighting?Cellular & molecular immunology · 2025Article
- Curcumin-Piperine Self-Nanoemulsifying Delivery inPharmaceuticals (Basel, Switzerland) · 2025Article
- Evaluating the Protective Effects of Silymarin Along with a Cholesterol-Supplemented Diet Against Demyelination in an EAE Mouse Model of Multiple Sclerosis: Lipidomic and Inflammatory Aspects.Molecular neurobiology · 2025Article
- The interplay between endoplasmic reticulum stress and inflammation in multiple sclerosis.Scientific reports · 2025Article
19 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
17 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a common neurological disorder of putative autoimmune origin. Clinical and experimental studies delineate abnormal expression of specific cytokines over the course of the disease. One major cytokine that has been shown to play a pivotal role in MS is tumor necrosis factor (TNF). TNF is a pleiotropic cytokine regulating many physiological and pathological functions of both the immune system and the central nervous system (CNS). Convincing evidence from studies in human and experimental MS have demonstrated the involvement of TNF in various pathological hallmarks of MS, including immune dysregulation, demyelination, synaptopathy and neuroinflammation. However, due to the complexity of TNF signaling, which includes two-ligands (soluble and transmembrane TNF) and two receptors, namely TNF receptor type-1 (TNFR1) and type-2 (TNFR2), and due to its cell- and context-differential expression, targeting the TNF system in MS is an ongoing challenge. This review summarizes the evidence on the pathophysiological role of TNF in MS and in different MS animal models, with a special focus on pharmacological treatment aimed at controlling the dysregulated TNF signaling in this neurological disorder.
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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.