ArticleJCI insight2017
GM-CSF is not essential for experimental autoimmune encephalomyelitis but promotes brain-targeted disease.
Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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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Who cites it
36 citing papers in PubMed, 45 citations in OpenAlex.
- IL-17A deficiency in HLA-DR3 transgenic mice enriches beneficial Prevotella species in gut to promote Tregs and reduce CNS autoimmunity.Microbiome · 2026Article
- CD11c+ CD8 T cells cause IFN-γ-dependent autoimmune neuroinflammation that is restrained by PD-1 signaling.JCI insight · 2026Article
- Single-cell RNA sequencing uncovers neutrophil clusters associated with autoimmune neuroinflammation.Journal of neuroinflammation · 2026Article
- Single-Cell RNA Sequencing Uncovers Neutrophil Clusters Associated with Autoimmune Neuroinflammation.Research square · 2025Article
- Migration arrest and transendothelial trafficking of human pathogenic-like Th17 cells are mediated by differentially positioned chemokines.Nature communications · 2025Article
- GM-CSFTheranostics · 2025Review
- Cytokines, Vascular Endothelial Growth Factors, and PlGF in Autoimmunity: Insights From Rheumatoid Arthritis to Multiple Sclerosis.Immune network · 2024Review
- The brain cytokine orchestra in multiple sclerosis: from neuroinflammation to synaptopathology.Molecular brain · 2024Review
- Formyl peptide receptor 2 regulates dendritic cell metabolism and Th17 cell differentiation during neuroinflammation.Frontiers in immunology · 2024Article
- RIPK3 promotes brain region-specific interferon signaling and restriction of tick-borne flavivirus infection.PLoS pathogens · 2023Article
- Chemokine positioning determines mutually exclusive roles for their receptors in extravasation of pathogenic human T cells.bioRxiv : the preprint server for biology · 2023Article
- B Cells Drive MHC Class I-Restricted CD4 T Cells to Induce Spontaneous Central Nervous System Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Neuroinflammation: Extinguishing a blaze of T cells.Immunological reviews · 2022Review
- Role of RGC-32 in multiple sclerosis and neuroinflammation - few answers and many questions.Frontiers in immunology · 2022Review
- Chemokine-Driven Migration of Pro-Inflammatory CD4Frontiers in immunology · 2022Review
- Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The hedgehog pathway suppresses neuropathogenesis in CD4 T cell-driven inflammation.Brain : a journal of neurology · 2021Article
- Colony stimulating factors in the nervous system.Seminars in immunology · 2021Review
- Cytokines and transcription factors in the differentiation of CD4Current opinion in immunology · 2020Review
- Autoimmunity to neuroretina in the concurrent absence of IFN-γ and IL-17A is mediated by a GM-CSF-driven eosinophilic inflammation.Journal of autoimmunity · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Experimental autoimmune encephalomyelitis (EAE) has been used as an animal model of multiple sclerosis to identify pathogenic cytokines that could be therapeutic targets. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is the only cytokine reported to be essential for EAE. We investigated the role of GM-CSF in EAE in C3HeB/FeJ mice that uniquely exhibit extensive brain and spinal cord inflammation. Unexpectedly, GM-CSF-deficient C3HeB/FeJ mice were fully susceptible to EAE because IL-17 activity compensated for the loss of GM-CSF during induction of spinal cord-targeted disease. In contrast, both GM-CSF and IL-17 were needed to fully overcome the inhibitory influence of IFN-γ on the induction of inflammation in the brain. Both GM-CSF and IL-17 independently promoted neutrophil accumulation in the brain, which was essential for brain-targeted disease. These results identify a GM-CSF/IL-17/IFN-γ axis that regulates inflammation in the central nervous system and suggest that a combination of cytokine-neutralizing therapies may be needed to dampen central nervous system autoimmunity.
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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.