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Publication Detail
Microbiota-Derived Metabolites Suppress Arthritis by Amplifying Aryl-Hydrocarbon Receptor Activation in Regulatory B Cells.
  • Publication Type:
    Journal article
  • Publication Sub Type:
  • Authors:
    Rosser EC, Piper CJM, Matei DE, Blair PA, Rendeiro AF, Orford M, Alber DG, Krausgruber T, Catalan D, Klein N, Manson JJ, Drozdov I, Bock C, Wedderburn LR, Eaton S, Mauri C
  • Publication date:
  • Journal:
    Cell Metab
  • Status:
    Published online
  • Country:
    United States
  • PII:
  • Language:
  • Keywords:
    5-Hydroxyindole-3-acetic acid, B cells, aryl-hydrocarbon receptor, autoimmunity, butyrate, regulatory B cells, rheumatoid arthritis, serotonin, short chain fatty acid, tryptophan metabolism
The differentiation of IL-10-producing regulatory B cells (Bregs) in response to gut-microbiota-derived signals supports the maintenance of tolerance. However, whether microbiota-derived metabolites can modulate Breg suppressive function remains unknown. Here, we demonstrate that rheumatoid arthritis (RA) patients and arthritic mice have a reduction in microbial-derived short-chain fatty acids (SCFAs) compared to healthy controls and that in mice, supplementation with the SCFA butyrate reduces arthritis severity. Butyrate supplementation suppresses arthritis in a Breg-dependent manner by increasing the level of the serotonin-derived metabolite 5-Hydroxyindole-3-acetic acid (5-HIAA), which activates the aryl-hydrocarbon receptor (AhR), a newly discovered transcriptional marker for Breg function. Thus, butyrate supplementation via AhR activation controls a molecular program that supports Breg function while inhibiting germinal center (GC) B cell and plasmablast differentiation. Our study demonstrates that butyrate supplementation may serve as a viable therapy for the amelioration of systemic autoimmune disorders.
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Infection, Immunity & Inflammation Dept
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