Abstract
Cellular autoimmunity is thought to be primarily responsible for the selective destruction of islet beta cells in Type I diabetes. Why the T lymphocyte reacts to self and recognizes the beta cell as foreign, as against the other endocrine islet cells, is unknown. One key issue is whether the beta cell itself is capable of presenting autoantigen(s) and thereby breaking T lymphocyte tolerance. In this paper we discuss current concepts of antigen presentation and relate these to recent findings from our laboratory, suggesting that the beta cell can be induced to display many of the phenotypic properties of classical antigen-presenting cells, including induction of MHC and ICAM-1 expression and production of IL-6. Finally, a model is presented which provides a new view of the initiation and perpetuation of autoimmune beta-cell destruction in Type I diabetes.
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