ReviewCritical reviews in immunology2015
Opportunities for Translation from the Bench: Therapeutic Intervention of the JAK/STAT Pathway in Neuroinflammatory Diseases.
Review in Critical reviews in immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed.
- The lung-brain axis in neurodegeneration: inflammatory, immune, and vascular mechanisms with therapeutic implications.Inflammopharmacology · 2026Review
- Reduced expression of SOCS1-5 and STAT5a genes in Parkinson's disease patients: evidence for dysregulated immune signaling.Molecular biology reports · 2026Article
- Integrated Transcriptomic and Machine Learning Analysis Reveals Immune-Related Regulatory Networks in Anti-NMDAR Encephalitis.International journal of molecular sciences · 2026Article
- Inflammatory bowel disease therapies and demyelinating diseases: a practical guide to therapeutic benefit and risk.Journal of Crohn's & colitis · 2026Review
- Environmental Stressors and Neuroinflammation: Linking Climate Change to Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Deliver CEBPE via cartilage targeting Lipid nanoparticle to block CEBPE-LTF-STAT3 positive feedback loop for efficient treatment of cartilage endplate degeneration.Materials today. Bio · 2025Article
- Tofacitinib Improves Motor Symptoms in Parkinsonism Associated with a Heterozygous NGLY1 Variant and Autoimmune Disease.European journal of case reports in internal medicine · 2025Article
- JAK-STAT Signaling in Autoimmunity and Cancer.ImmunoTargets and therapy · 2025Review
- Mechanisms and Emerging Regulators of Neuroinflammation: Exploring New Therapeutic Strategies for Neurological Disorders.Current issues in molecular biology · 2024Review
- Astrocytic DLL4-NOTCH1 signaling pathway promotes neuroinflammation via the IL-6-STAT3 axis.Journal of neuroinflammation · 2024Article
- Suppression of the JAK/STAT pathway inhibits neuroinflammation in the line 61-PFF mouse model of Parkinson's disease.Journal of neuroinflammation · 2024Article
- Exploring the clinical transition of engineered exosomes designed for intracellular delivery of therapeutic proteins.Stem cells translational medicine · 2024Review
- Article
- Suppression of the JAK/STAT Pathway Inhibits Neuroinflammation in the Line 61-PFF Mouse Model of Parkinson's Disease.Research square · 2024Article
- JAK-STAT signaling in inflammation and stress-related diseases: implications for therapeutic interventions.Molecular biomedicine · 2023Review
- Molecular Mechanisms Underlying Neuroinflammation Elicited by Occupational Injuries and Toxicants.International journal of molecular sciences · 2023Review
- In Silico Drug Repurposing in Multiple Sclerosis Using scRNA-Seq Data.International journal of molecular sciences · 2023Article
- Role of JAK/STAT in the Neuroinflammation and its Association with Neurological Disorders.Annals of neurosciences · 2021Review
- Review
- Interleukin-19 Abrogates Experimental Autoimmune Encephalomyelitis by Attenuating Antigen-Presenting Cell Activation.Frontiers in immunology · 2021Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Pathogenic CD4+ T cells and myeloid cells play critical roles in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), an animal model of MS. These immune cells secrete aberrantly high levels of pro-inflammatory cytokines that pathogenically bridge the innate and adaptive immune systems and damage neurons and oligodendrocytes. These cytokines include interleukin-2 (IL-2), IL-6, IL-12, IL-21, IL-23, granulocyte macrophage-colony stimulating factor (GM-CSF), and interferon-γ (IFN-γ). It is, therefore, not surprising that both the dysregulated expression of these cytokines and the subsequent activation of their downstream signaling cascades is a common feature in MS/EAE. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway is utilized by numerous cytokines for signal transduction and is essential for the development and regulation of immune responses. Unbridled activation of the JAK/STAT pathway by pro-inflammatory cytokines has been demonstrated to be critically involved in the pathogenesis of MS/EAE. In this review, we discuss recent advancements in our understanding of the involvement of the JAK/STAT signaling pathway in the pathogenesis of MS/EAE, with a particular focus on therapeutic approaches to target the JAK/STAT pathway.
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Registered trials
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