ArticleProceedings of the National Academy of Sciences of the United States of America2016
Obeticholic acid, a synthetic bile acid agonist of the farnesoid X receptor, attenuates experimental autoimmune encephalomyelitis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. 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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Who cites it
41 citing papers in PubMed, 82 citations in OpenAlex.
- Obeticholic acid attenuates complete freund's adjuvant-induced arthritis in rats through FXR-mediated modulation of TGF-β/TAK1/MKK3/p38 MAPK signaling, inflammation, and oxidative stress.Inflammopharmacology · 2026Article
- CAR-T Cell Therapy and Gut Microbiota Modulation in Multiple Sclerosis: Emerging Therapeutic Strategies and Current Limitations.Current issues in molecular biology · 2026Review
- Microbiota-gut-brain axis and bile acids-driven neuromodulation.Neural regeneration research · 2026Article
- Regulation of Tph cell differentiation via farnesoid X receptor of dendritic cells in inflammatory bowel disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Farnesol, the farnesol pathway, and the immune-gut-brain axis.Frontiers in pharmacology · 2026Review
- Gut microbiota and gut-derived metabolites in defining multiple sclerosis phenotypic continuum.Frontiers in immunology · 2026Review
- Research progress on the role of gut microbiota dysbiosis in the pathogenesis of immune-mediated liver diseases.Frontiers in immunology · 2026Review
- Unraveling multiple sclerosis: a hidden interaction between intestinal microbiota and host lipid metabolism.Gut microbes · 2025Review
- Emerging Roles of Bile Acids in Neuroinflammation.International journal of molecular sciences · 2025Review
- Farnesoid X Receptor Alleviates Cisplatin-Induced Kidney Inflammatory Injury by Inhibiting Tlr4/NF-κB Pathway.Journal of cellular and molecular medicine · 2025Article
- The gut microbiota-bile acid axis: a crucial regulator of immune function and metabolic health.World journal of microbiology & biotechnology · 2025Review
- Microbiota-produced immune regulatory bile acid metabolites control central nervous system autoimmunity.Cell reports. Medicine · 2025Article
- Double-negative T cells in combination with ursodeoxycholic acid ameliorates immune-mediated cholangitis in mice.BMC medicine · 2025Article
- Bile's Hidden Weapon: Modulating the Microbiome and Tumor Microenvironment.Current microbiology · 2024Review
- Activation of Nrf2 and FXR via Natural Compounds in Liver Inflammatory Disease.International journal of molecular sciences · 2024Review
- Gut-Brain Interactions and Their Impact on Astrocytes in the Context of Multiple Sclerosis and Beyond.Cells · 2024Review
- Mitochondrial and metabolic dysfunction of peripheral immune cells in multiple sclerosis.Journal of neuroinflammation · 2024Review
- Bile acid metabolomics identifies chenodeoxycholic acid as a therapeutic agent for pancreatic necrosis.Cell reports. Medicine · 2023Article
- Article
- The activity of the aryl hydrocarbon receptor in T cells tunes the gut microenvironment to sustain autoimmunity and neuroinflammation.PLoS biology · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bile acids are ligands for the nuclear hormone receptor, farnesoid X receptor (FXR). The bile acid-FXR interaction regulates bile acid synthesis, transport, and cholesterol metabolism. Recently, bile acid-FXR regulation has been reported to play an integral role in both hepatic and intestinal inflammation, and in atherosclerosis. In this study, we found that FXR knockout mice had more disease severity in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Obeticholic acid (6α-ethyl-chenodeoxycholic acid, 6-ECDCA), a synthetic FXR agonist, is an orally available drug that is currently in clinical trials for the treatment of inflammatory diseases such as alcoholic hepatitis, nonalcoholic steatohepatitis, and primary biliary cirrhosis. When we treated mice exhibiting established EAE with 6-ECDCA, or the natural FXR ligand chenodeoxycholic acid (CDCA), clinical disease was ameliorated by (i) suppressing lymphocyte activation and proinflammatory cytokine production; (ii) reducing CD4(+) T cells and CD19(+) B cell populations and their expression of negative checkpoint regulators programmed cell death protein 1 (PD1), programmed death-ligand 1 (PD-L1), and B and T lymphocyte attenuator (BTLA); (iii) increasing CD8(+) T cells and PD1, PDl-1, and BTLA expression; and (iv) reducing VLA-4 expression in both the T- and B-cell populations. Moreover, adoptive transfer of 6-ECDCA- or CDCA-treated donor cells failed to transfer disease in naive recipients. Thus, we show that FXR functions as a negative regulator in neuroinflammation and we highlight that FXR agonists represent a potential previously unidentified therapy for MS.
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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.