Abstract
Organ-specific autoimmunity has been recognised in virtually all the defined endocrine glands, where it is the hormone-producing epithelial cells themselves which are destroyed. The mechanisms leading to this breakdown of self-tolerance are still unknown, although a variety of hypotheses have been proposed (reviewed in 1 and 2). Two requirements which may well be central to these mechanisms are the accessibility of autoantigens to cells of the immune system, and the presentation of such antigens in an immunogenic fashion. In recent years we have performed a variety of experiments relevant to these points, mainly in thyroid autoimmunity, in which there is marked lymphocytic infiltration of the gland, including activated T cells (3). Our results have led to a general model for the generation of organ-specific endocrine autoimmunity. Central to this hypothesis is the ability of endocrine epithelial cells to present their own surface molecules as autoantigens.
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Todd, I., Londei, M., Pujol-Borrell, R., Feldmann, M., Bottazzo, G.F. (1985). Can Epithelial Cells Present Surface Autoantigens?. In: Feldmann, M., Mitchison, N.A. (eds) Immune Regulation. Experimental Biology and Medicine, vol 8. Humana Press. https://doi.org/10.1007/978-1-4612-4996-2_39
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DOI: https://doi.org/10.1007/978-1-4612-4996-2_39
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