medwireNews: Commensal bacteria may be involved in triggering systemic lupus erythematosus (SLE) in genetically predisposed individuals, results of a proof-of-concept study suggest.
As reported in Science Translational Medicine, bacteria taken from skin, mouth, and stool samples of 13 patients with SLE and seven healthy controls contained orthologs of the human protein Ro60. Eight of the SLE patients had autoantibodies to Ro60.
“Almost all patients with SLE have high titers of anti-nuclear autoantibodies, which can be detected years before the onset of symptoms,” and anti-Ro60 “is the earliest and most common” such antibody, explain Martin Kriegel (Yale University School of Medicine, New Haven, Connecticut, USA) and study co-authors.
In immunoprecipitation experiments, the researchers found that serum samples from the Ro60 autoantibody-positive SLE patients reacted with cultured commensal bacteria, but samples from the SLE patients without Ro60 autoantibodies and healthy controls did not.
And T cells from the anti–Ro60-positive patients were activated in vitro by the Ro60 ortholog from commensal bacteria, suggesting that “microbiota-reactive T cell clones […] could initiate Ro60 autoreactivity in vivo,” say Kriegel and team.
Furthermore, lupus-prone mice colonized with bacteria containing the Ro60 ortholog developed an immune response to the protein and showed SLE-like symptoms.
“Together, these data suggest that Ro60 orthologs from human commensal bacteria may initiate and drive lupus pathogenesis,” conclude the study authors.
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