ArticleScientific reports2020
Anxiolytic Drug FGIN-1-27 Ameliorates Autoimmunity by Metabolic Reprogramming of Pathogenic Th17 Cells.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- The Pathogenic Role of T Cell Metabolism and its Effect on Immune Senescence in Autoimmune Diseases and Infection.Clinical reviews in allergy & immunology · 2025Review
- Single cell resolution of neurosteroidogenesis in the murine brain: de novo biosynthesis.The Journal of endocrinology · 2025Article
- Transient anxiety-and depression-like behaviors are linked to the depletion of Foxp3-expressing cells via inflammasome in the brain.PNAS nexus · 2023Article
- In Silico Drug Repurposing in Multiple Sclerosis Using scRNA-Seq Data.International journal of molecular sciences · 2023Article
- Mitochondrial translocator protein deficiency exacerbates pathology in acute experimental ulcerative colitis.Frontiers in physiology · 2022Article
- Identification of Small Molecule Inhibitors of a Mir155 Transcriptional Reporter in Th17 Cells.Scientific reports · 2021Article
- The Effects of Adoptively Transferred IL-23/IL-18-Polarized Neutrophils on Tumor and Collagen-Induced Arthritis in Mice.Journal of inflammation research · 2021Article
- Lack of adrenal TSPO/PBR expression in hamsters reinforces correlation to triglyceride metabolism.The Journal of endocrinology · 2020Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Th17 cells are critical drivers of autoimmune diseases and immunopathology. There is an unmet need to develop therapies targeting pathogenic Th17 cells for the treatment of autoimmune disorders. Here, we report that anxiolytic FGIN-1-27 inhibits differentiation and pathogenicity of Th17 cells in vitro and in vivo using the experimental autoimmune encephalomyelitis (EAE) model of Th17 cell-driven pathology. Remarkably, we found that the effects of FGIN-1-27 were independent of translocator protein (TSPO), the reported target for this small molecule, and instead were driven by a metabolic switch in Th17 cells that led to the induction of the amino acid starvation response and altered cellular fatty acid composition. Our findings suggest that the small molecule FGIN-1-27 can be re-purposed to relieve autoimmunity by metabolic reprogramming of pathogenic Th17 cells.
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Registered trials
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