VIRUSES, CYTOKINES, ANTIGENS, AND AUTOIMMUNITY

To explain the pathogenesis of autoimmunity, we hypothesize that follo wing an infection the immune response spreads to tissue-specific autoa ntigens in genetically predisposed individuals eventually determining progression to disease. Molecular mimicry between viral and self antig ens could, in some instances, initiate autoimmunity. Local elicitation of inflammatory cytokines following infection probably plays a pivota l role in determining loss of functional tolerance to self autoantigen s and the destructive activation of autoreactive cells. We also descri be the potential role of interleukin 10, a powerful B-cell activator, in increasing the efficiency of epitope recognition, that could well b e crucial to the progression toward disease.