Abstract
Evidence is presented which supports the suggestion that whether a given antigen is vulnerable to an autoimmune attack is dependent upon the specific immune status of B cells and T cells to that antigen which, in turn, is dictated by the concentration of self antigen in their microenvironment. That B cells require much higher concentrations of self antigens than do T cells for the maintenance of tolerance is supported by data presented using an experimental model of acquired tolerance to serum proteins. Depending on the immune status of T cells and B cells to self antigen, the following three models are suggested for the early events leading to autoimmunity: 1) polyclonal activation of competent B cells, 2) direct activation of competent T cells, and 3) bypass of specifically tolerant T cells and activation of competent B cells. The role of a regulatory network involving the suppressor cell circuit in the induction and regulation of autoimmunity is discussed.
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