ArticleACR open rheumatology2025
Gut Expansion of a Human Lupus Pathobiont is Associated With Autoantibody Production and T Cell Dysregulation.
Article in ACR open rheumatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Hepatic control of immunometabolism: implications for the pathogenesis, diagnosis and treatment of rheumatic diseases.Nature reviews. Rheumatology · 2026Review
- A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis.Annals of the rheumatic diseases · 2026Article
- Multiomics-guided discovery of protective microbiome signatures in lupus-prone mice treated with Faecalibacterium prausnitzii.Nature communications · 2026Article
- Autoimmune disease-associated pathobionts: mechanisms and therapeutic potential of phage-based approaches.Frontiers in immunology · 2026Review
- Pathogenic strains of a gut commensal drive systemic platelet activation and thromboinflammation in lupus nephritis.bioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
objectiveThe mechanisms by which the gut microbiome contributes to lupus pathogenesis remain poorly understood. The anaerobe Ruminococcus gnavus (RG) expands in patients with lupus in association with flares. The goal of this study was to determine the mechanisms by which candidate pathobiont lipoglycan-producing RG2 may contribute to autoimmunity and to identify factors promoting its expansion.
methodsThe consequences of RG colonization or depletion were evaluated in the B6.Sle1.Sle2.Sle3 triple congenic (TC) lupus model by flow cytometry and enzyme-linked immunosorbent assay. RG lysates were tested on Treg cells in vitro. Fecal microbiota transfers evaluated the contribution of the microbiome origin from lupus or control donors and dietary tryptophan. RG1 and RG2 growth and metabolome were evaluated in response to tryptophan in vitro.
resultsOnly RG2 stably colonized TC mice, in which it induced autoantibody production and T cell activation. Depletion of anaerobes had the opposite effect, with an increased Treg frequency. RG2 induced Treg apoptosis in cocultures with dendritic cells. RG is present in TC microbiota, from which it is amplified by tryptophan. The combination of TC microbiota and high dietary tryptophan induced autoimmune activation and intestinal inflammation in healthy control mice. Finally, tryptophan enhanced RG2 growth and production of immunomodulatory metabolites.
conclusionRG2 contributes to autoimmune activation, at least by inducing Treg apoptosis. The expansion of this pathobiont is promoted by host genetic factors and tryptophan metabolism. Thus, targeted RG2 depletion may improve disease outcomes in patients with lupus.
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Registered trials
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