Extracellular Vesicles Derived From Streptococcus anginosus Aggravate Lupus Nephritis by Triggering TLR2-MyD88-NF-κB Signalling in NK Cells.

ABSTRACT: Systemic lupus erythematosus (SLE) has been linked to gut microbiome dysbiosis, notably an overabundance of Streptococcus anginosus; however, the impact of this microbial imbalance on disease pathogenesis remains unclear. Here, we investigated the contribution of S. anginosus-derived extracellular vesicles (SA-EVs) to SLE progression, with an emphasis on lupus nephritis (LN). Fifty-four SLE patients and 43 healthy controls (HC) were recruited. The faecal, blood and serum samples from participants were collected. SLE disease activity (SLEDA) was evaluated by the SLEDA Index (SLEDAI). Stool S. anginosus abundance was quantified by quantitative PCR, NK cell activation by flow cytometry and serum proinflammatory cytokines profile by ELISA. Lupus-prone MRL/lpr mice were orally administered SA-E

SUBMITTER: Gong Y 

PROVIDER: S-EPMC12269530 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature