• 1 June 1988
    • journal article
    • review article
    • Vol. 20, 3-10
Abstract
Our concepts of autoimmune disease have evolved with our changing understanding of the immune response. In recent years, clonal deletion theories have gradually given way to more dynamic views of the regulation of anti-self immune reactions. It is now clear that self-reactive B cells and some self-reactive T cells persist in the body, and there is every reason to believe that antigen-presenting cells are fully capable of presenting self-antigens in the same manner as foreign antigens. The critical event in the induction of autoimmune disease, therefore, is the quantitative balance of active suppression v the induction of self-reactive help. This help provided a helper T cell response requires that the self-antigens be presented in the context of self-MHC with sufficient affinity and avidity. The antireaction must be potent enough to overcome the totality of suppressive factors, including specific and non-specific suppressor T cells and anti-idiotypic or anti-T-cell-receptor responses.

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