Evidence map›Paper›PMID 32213346›Full record

ArticleCell metabolism2020

Microbiota-Derived Metabolites Suppress Arthritis by Amplifying Aryl-Hydrocarbon Receptor Activation in Regulatory B Cells.

Elizabeth C Rosser, Christopher J M Piper, Diana E Matei, Paul A Blair, André F Rendeiro, Michael Orford, Dagmar G Alber, Thomas Krausgruber, Diego Catalan, Nigel Klein and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Cell metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 336 papers, 8 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
336citing papers in PubMed, 8 pooled it
25.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

336 citing papers in PubMed, 8 syntheses or guidelines pooled it, 537 citations in OpenAlex.

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  15. A guide to B cell metabolism.Nature reviews. Immunology · 2026
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276 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 7 institutions in 4 countries.

Elizabeth C RosserCentre for Adolescent Rheumatology Versus Arthritis at UCL, UCLH and GOSH, London, UK; Centre for Rheumatology Research, Division of Medicine, UCL, London WC1E 6JF, UK; Infection, Immunity and Inflammation Programme, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK. Electronic address: e.rosser@ucl.ac.uk.
Christopher J M PiperCentre for Rheumatology Research, Division of Medicine, UCL, London WC1E 6JF, UK.
Diana E MateiCentre for Rheumatology Research, Division of Medicine, UCL, London WC1E 6JF, UK.
Paul A BlairCentre for Rheumatology Research, Division of Medicine, UCL, London WC1E 6JF, UK.
André F RendeiroCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Michael OrfordDevelopmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK.
Dagmar G AlberInfection, Immunity and Inflammation Programme, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK.
Thomas KrausgruberCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
Diego CatalanCentre for Adolescent Rheumatology Versus Arthritis at UCL, UCLH and GOSH, London, UK; Programa Disciplinario de Inmunología, Facultad de Medicina, Instituto de Ciencias Biomédicas (ICBM), Universidad de Chile, Santiago, Chile.
Nigel KleinInfection, Immunity and Inflammation Programme, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK.
Jessica J MansonCentre for Adolescent Rheumatology Versus Arthritis at UCL, UCLH and GOSH, London, UK; Department of Rheumatology, University College Hospital, London, UK.
Ignat DrozdovBering Limited, London TW2 6EA, UK.
Christoph BockCeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria; Department of Laboratory Medicine, Medical University of Vienna, Vienna, Austria; Max Planck Institute for Informatics, Saarland Informatics Campus, Saarbrücken, Germany.
Lucy R WedderburnCentre for Adolescent Rheumatology Versus Arthritis at UCL, UCLH and GOSH, London, UK; Infection, Immunity and Inflammation Programme, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK; NIHR Biomedical Research Centre at Great Ormond Street Hospital, London, UK.
Simon EatonDevelopmental Biology and Cancer Programme, UCL Great Ormond Street Institute of Child Health, London WC1N 1EH, UK.
Claudia MauriCentre for Rheumatology Research, Division of Medicine, UCL, London WC1E 6JF, UK. Electronic address: c.mauri@ucl.ac.uk.
Great Ormond Street Hospital · GBUniversity College London · GBAustrian Academy of Sciences · ATBritish Society for Rheumatology · GBCeMM Research Center for Molecular Medicine · ATUniversity College Hospital · GBVersus Arthritis · GB

Funding

Medical Research Council MR/M004600/1Medical Research Council MR/R013926/1Medical Research Council MR/T000910/1Versus Arthritis 21140Versus Arthritis 21141Versus Arthritis 21226Versus Arthritis 21257Versus Arthritis 21593
6 · The paper itself

Abstract

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.

Indexed as

Basic Helix-Loop-Helix ProteinsReceptors, Aryl HydrocarbonAnimalsArthritis, RheumatoidB-Lymphocytes, RegulatoryButyratesCells, CulturedFatty Acids, VolatileFemaleGastrointestinal MicrobiomeHumansHydroxyindoleacetic AcidMaleMiceMice, Inbred C57BLMiddle AgedAhr protein, mouseBasic Helix-Loop-Helix ProteinsButyratesFatty Acids, VolatileHydroxyindoleacetic AcidReceptors, Aryl Hydrocarbon5-Hydroxyindole-3-acetic acidaryl-hydrocarbon receptorautoimmunityB cellsbutyrateregulatory B cellsrheumatoid arthritisserotoninshort chain fatty acidtryptophan metabolism

Identifiers

PMID32213346
PMCPMC7156916
OpenAlexW3013317600

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.