ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Th Cell Diversity in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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.
The trial behind it
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Who cites it
41 citing papers in PubMed.
- Alternatively activated neutrophils limit T cell-driven neuroinflammation.Journal of neuroinflammation · 2026Article
- GM-CSFTheranostics · 2025Review
- The Functional Interaction Between Epstein-Barr Virus and MYC in the Pathogenesis of Burkitt Lymphoma.Cancers · 2024Review
- 25 Hydroxyvitamin D and Cytokine Profile in Patients With Relapsing-Remitting Multiple Sclerosis.Cureus · 2024Article
- BHLHE40 Mediates Cross-Talk between Pathogenic TH17 Cells and Myeloid Cells during Experimental Autoimmune Encephalomyelitis.ImmunoHorizons · 2023Article
- Histamine H4 Receptor Antagonist Ameliorates the Progression of Experimental Autoimmune Encephalomyelitis via Regulation of T-Cell Imbalance.International journal of molecular sciences · 2023Article
- Synthesis and Comprehensive in Vivo Activity Profiling of Olean-12-en-28-ol, 3β-Pentacosanoate in Experimental Autoimmune Encephalomyelitis: A Natural Remyelinating and Anti-Inflammatory Agent.Journal of natural products · 2023Article
- Utility of the visual system to monitor neurodegeneration in multiple sclerosis.Frontiers in molecular neuroscience · 2023Review
- Neuroinflammation: Extinguishing a blaze of T cells.Immunological reviews · 2022Review
- Biological Sex As a Critical Variable in CD4Antioxidants & redox signaling · 2022Review
- Visual imaging as a predictor of neurodegeneration in experimental autoimmune demyelination and multiple sclerosis.Acta neuropathologica communications · 2022Article
- LncRNA RUNX1-IT1 affects the differentiation of Th1 cells by regulating NrCAM transcription in Graves' disease.Cell cycle (Georgetown, Tex.) · 2022Article
- Effects of biological sex and pregnancy in experimental autoimmune encephalomyelitis: It's complicated.Frontiers in immunology · 2022Review
- Brain Antigens Stimulate Proliferation of T Lymphocytes With a Pathogenic Phenotype in Multiple Sclerosis Patients.Frontiers in immunology · 2022Article
- Th17-Related Cytokines as Potential Discriminatory Markers between Neuromyelitis Optica (Devic's Disease) and Multiple Sclerosis-A Review.International journal of molecular sciences · 2021Review
- Should mast cells be considered therapeutic targets in multiple sclerosis?Neural regeneration research · 2020Review
- The Potential Contribution of Dysfunctional RNA-Binding Proteins to the Pathogenesis of Neurodegeneration in Multiple Sclerosis and Relevant Models.International journal of molecular sciences · 2020Review
- GM-CSF in inflammation.The Journal of experimental medicine · 2020Review
- Pathogenic T cell cytokines in multiple sclerosis.The Journal of experimental medicine · 2020Review
- Transient Expression of IL-17A in Foxp3 Fate-Tracked Cells inFrontiers in immunology · 2020Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Multiple sclerosis (MS) is believed to be initiated by myelin-reactive CD4(+) Th cells. IL-12-polarized Th1 cells, IL-23-polarized Th17 cells, and Th17 cells that acquire Th1 characteristics were each implicated in autoimmune pathogenesis. It is debated whether Th cells that can drive the development of demyelinating lesions are phenotypically diverse or arise from a single lineage. In the current study, we assessed the requirement of IL-12 or IL-23 stimulation, as well as Th plasticity, for the differentiation of T cells capable of inducing CNS axon damage. We found that stable murine Th1 and Th17 cells independently transfer experimental autoimmune encephalomyelitis (widely used as an animal model of MS) in the absence of IL-23 and IL-12, respectively. Plastic Th17 cells are particularly potent mediators of demyelination and axonopathy. In parallel studies, we identified MS patients who consistently mount either IFN-γ- or IL-17-skewed responses to myelin basic protein over the course of a year. Brain magnetic resonance imaging revealed that patients with mixed IFN-γ and IL-17 responses have relatively high T1 lesion burden, a measure of permanent axon damage. Our data challenge the dogma that IL-23 and Th17 plasticity are universally required for the development of experimental autoimmune encephalomyelitis. This study definitively demonstrates that autoimmune demyelinating disease can be driven by distinct Th-polarizing factors and effector subsets, underscoring the importance of a customized approach to the pharmaceutical management of MS.
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