ArticleCell2020
Cell Type-Specific Intralocus Interactions Reveal Oligodendrocyte Mechanisms in MS.
Article in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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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
25 citing papers in PubMed.
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025Review
- A focus on the normal-appearing white and gray matter within the multiple sclerosis brain: a link to smoldering progression.Acta neuropathologica · 2025Review
- Epigenetic and Mitochondrial Metabolic Dysfunction in Multiple Sclerosis: A Review of Herbal Drug Approaches and Current Clinical Trials.Molecular neurobiology · 2025Review
- Improving polygenic prediction from whole-genome sequencing data by leveraging predicted epigenomic features.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Patient iPSC models reveal glia-intrinsic phenotypes in multiple sclerosis.Cell stem cell · 2024Article
- Combined transcriptomics and proteomics studies on the effect of electrical stimulation on spinal cord injury in rats.Heliyon · 2024Article
- Cytotoxic CNS-associated T cells drive axon degeneration by targeting perturbed oligodendrocytes iniScience · 2023Article
- Genetic insights into immune mechanisms of Alzheimer's and Parkinson's disease.Frontiers in immunology · 2023Review
- Nested epistasis enhancer networks for robust genome regulation.Science (New York, N.Y.) · 2022Article
- Multiple sclerosis genetic and non-genetic factors interact through the transient transcriptome.Scientific reports · 2022Article
- Epigenomic priming of immune genes implicates oligodendroglia in multiple sclerosis susceptibility.Neuron · 2022Article
- Central nervous system regeneration: the roles of glial cells in the potential molecular mechanism underlying remyelination.Inflammation and regeneration · 2022Review
- Lesion features on magnetic resonance imaging discriminate multiple sclerosis patients.European journal of neurology · 2022Article
- Activation of glucagon-like peptide-1 receptor in microglia attenuates neuroinflammation-induced glial scarring via rescuing Arf and Rho GAP adapter protein 3 expressions after nerve injury.International journal of biological sciences · 2022Article
- Sustained ErbB Activation Causes Demyelination and Hypomyelination by Driving Necroptosis of Mature Oligodendrocytes and Apoptosis of Oligodendrocyte Precursor Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Multiple Sclerosis Phenotypes as a Continuum: The Role of Neurologic Reserve.Neurology. Clinical practice · 2021Review
- Diversity and Function of Glial Cell Types in Multiple Sclerosis.Trends in immunology · 2021Review
- The β-Cell Genomic Landscape in T1D: Implications for Disease Pathogenesis.Current diabetes reports · 2021Review
- Editorial: "Inside-Out" vs "Outside-In" Paradigms in Multiple Sclerosis Etiopathogenesis.Frontiers in cellular neuroscience · 2021Article
Corrections and comments
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Authors and funding
28 authors.
Funding
Abstract
Multiple sclerosis (MS) is an autoimmune disease characterized by attack on oligodendrocytes within the central nervous system (CNS). Despite widespread use of immunomodulatory therapies, patients may still face progressive disability because of failure of myelin regeneration and loss of neurons, suggesting additional cellular pathologies. Here, we describe a general approach for identifying specific cell types in which a disease allele exerts a pathogenic effect. Applying this approach to MS risk loci, we pinpoint likely pathogenic cell types for 70%. In addition to T cell loci, we unexpectedly identified myeloid- and CNS-specific risk loci, including two sites that dysregulate transcriptional pause release in oligodendrocytes. Functional studies demonstrated inhibition of transcriptional elongation is a dominant pathway blocking oligodendrocyte maturation. Furthermore, pause release factors are frequently dysregulated in MS brain tissue. These data implicate cell-intrinsic aberrations outside of the immune system and suggest new avenues for therapeutic development. VIDEO ABSTRACT.
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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.