Abstract
Systemic lupus erythematosus (SLE or lupus) is a polygenic syndrome of immunity against nuclear autoantigens. Recent data from several fields now suggest 'pseudoviral' immunity as a novel disease concept. Known lupus risk factors commonly compromise those mechanisms that protect chromatin and ribonucleoprotein particles from activating viral nucleic acid sensors. This process activates antigen-presenting cells and induces type I interferons. These central mediators of antiviral immunity have similar proinflammatory roles in lupus, explaining overlapping clinical manifestations, immunopathology and ultrastructural abnormalities in systemic viral infection and lupus. Structurally, chromatin and ribonucleoprotein particles resemble viral particles and have a similar potency to trigger antigen-specific B- and T-cell responses. Therefore, self nucleic acid-driven 'pseudoviral' immunity is evolving as another concept in understanding the pathogenesis of lupus and may offer novel targets for therapy.
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