ArticleJournal of neuroinflammation2023
GPR43 stimulation on TCRαβ
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- FFAR2 activation induces IL-22-dependent intestinal immune responses to suppress CNS autoimmunity.EMBO molecular medicine · 2026Article
- Migration of immune cells in tumors and inflammation: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Review
- Mechanistic insights from experimental autoimmune encephalomyelitis into immune regulation, autophagy, gut microbiota, blood-brain barrier integrity, and NLRP3 inflammasome-mediated pyroptosis in multiple sclerosis: potential clinical implications.Frontiers in neuroscience · 2026Review
- Artificial intelligence empowers gut microbiota research in neurodegenerative diseases molecular mechanisms and precision therapy.iScience · 2025Review
- Interactions between the gut microbiota and immune cell dynamics: novel insights into the gut-bone axis.Gut microbes · 2025Review
- Short-chain fatty acids are a key mediator of gut microbial regulation of T cell trafficking and differentiation after traumatic brain injury.Experimental neurology · 2025Article
- Intestinal mucosal immunity and type 1 diabetes: Non-negligible communication between gut and pancreas.Diabetes, obesity & metabolism · 2025Review
- Free Fatty Acids and Free Fatty Acid Receptors: Role in Regulating Arterial Function.International journal of molecular sciences · 2024Review
- Identification of master regulator genes controlling pathogenic CD4Scientific reports · 2024Article
- Increased regulatory activity of intestinal innate lymphoid cells type 3 (ILC3) prevents experimental autoimmune encephalomyelitis severity.Journal of neuroinflammation · 2024Article
- The emerging roles of microbiome and short-chain fatty acids in the pathogenesis of bronchopulmonary dysplasia.Frontiers in cellular and infection microbiology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
introductionGut microbiota plays a critical role in the regulation of immune homeostasis. Accordingly, several autoimmune disorders have been associated with dysbiosis in the gut microbiota. Notably, the dysbiosis associated with central nervous system (CNS) autoimmunity involves a substantial reduction of bacteria belonging to Clostridia clusters IV and XIVa, which constitute major producers of short-chain fatty acids (SCFAs). Here we addressed the role of the surface receptor-mediated effects of SCFAs on mucosal T-cells in the development of CNS autoimmunity.
methodsTo induce CNS autoimmunity, we used the mouse model of experimental autoimmune encephalomyelitis (EAE) induced by immunization with the myelin oligodendrocyte glycoprotein (MOG)-derived peptide (MOG
resultsOur results show a sharp and selective reduction of intestinal propionate at the peak of EAE development, accompanied by increased IFN-γ and decreased IL-22 in the colonic mucosa. Further analyses indicated that GPR43 was the primary SCFAs receptor expressed on T-cells, which was downregulated on colonic TCRαβ
conclusionsThese findings provide a novel mechanism involved in the gut-brain axis by which bacterial-derived products secreted in the gut mucosa might control the CNS tropism of autoreactive T-cells. Moreover, this study shows GPR43 expressed on T-cells as a promising therapeutic target for CNS 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.