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A study by Pianta et al published in the Journal of Clinical Investigation provides new evidence that the pathogenesis of rheumatoid arthritis (RA) may involve molecular mimicry, one of the most venerable models for the aetiology of rheumatic disease.1 Molecular mimicry represents the development of cross-reactive B or T cell responses to a component of an infecting agent. As shown in this study, the agent in question may be a commensal in the gut microbiome rather than a bacterium or virus inducing clinical disease.
While a violation of tolerance, molecular mimicry can occur due to the sharing of amino sequences by proteins from pathogen and host. If an immune response during infection goes awry, autoreactivity to the shared sequence can ensue. The most dramatic example of molecular mimicry is acute rheumatic fever (ARF), still a major problem worldwide. The scenario is now classic: within weeks of an infection with group A Streptococcus, usually pharyngitis, an inflammatory syndrome encompassing arthritis strikes a susceptible person. In ARF, the infection is obvious; the culprit bacterial antigen is the M protein.2
In a novel approach to finding molecular mimics, Pianta et al …
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