Lupus & antiphospholipid syndrome
A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis
Authors' conclusion
Gut expansions of the RG pathobiont may contribute to autoimmune pathogenesis through the LG toxin and cause LN flares through thromboinflammatory mechanisms in this previously unrecognised LN endotype.
Study context
- Population
- Patients with biopsy-proven lupus nephritis (LN), subsetted by gut microbiota community (Pilot cohort), plus an LN Validation cohort; murine modelsPilot and Validation LN cohorts
- Comparison
- Ruminococcus gnavus (RG) gut expansion / lipoglycan (LG) exposure vs without, in patients with LN and in mice
- Outcome
- Thromboinflammatory immune status: blood transcriptomic profiles, serum host proteins, anti-LG IgG, platelet function and tissue histology
Methodological detailstwo patient cohorts (Pilot, Validation), murine models
- Two patient cohorts (Pilot, Validation)
- Murine models
Main finding
As reported in the abstract
- RG gut expansions associated with high-level platelet, neutrophil, and monocyte activation
- Serum platelet factor 4 and NET release significantly higher with high anti-LG IgG
- anti-LG IgG a marker of in vivo immune exposure
Further findings
Validation LN cohort
- Confirmed these correlates; anti-LG antibodies serve as a surrogate for thromboinflammatory profile in this LN-associated endotype
Murine models
- Gut colonisation with LG-producing RG strains or a single LG injection caused megakaryocytosis and platelet activation
- RG colonisation with LG-producing strains induced tubulointerstitial injury with NETosis
- In vivo responses to LG toxin were Toll-like receptor 2-dependent
Original publication
A pathogenic gut lipoglycan drives systemic thromboinflammation in lupus nephritis. Ann Rheum Dis. Published 23 April 2026. doi:10.
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