Abstract
Self-tolerance may be mediated by pre-programmed rather than by antigen-driven mechanisms. Failure of differentiation macromolecules to associate with Ia molecules would provide one such mechanism. Inappropriate association could occur through macrophage reprocessing, and could be an important cause of autoimmune disease. Analysis of the response of mice to alloantigens provides evidence of limited antigen reprocessing. The hypothesis accounts for the chronic nature of autoimmune disease in terms of activation of latent help.
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