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Molecular Biology of β-Cell Destruction by Autoimmune Processes

  • Chapter
Type 1 Diabetes

Part of the book series: Contemporary Endocrinology ((COE))

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Abstract

The development of type 1 diabetes is closely related to the disappearance of β-cells from the islets of Langerhans. Loss of β-cells was already documented in the beginning of the last century when patients died from diabetes prior to the discovery of insulin. As pointed out by Gepts (1), authors also described inflammatory cells in the islets of Langerhans, but it was not until the post-insulin-discovery era that the inflammatory lesion was referred to as insulitis (2). The rediscovery of insulitis combined with rigorous morphometric analyses of β-cell loss by Gepts (1) was crucial to emerging views that, in fact, insulin-dependent diabetes mellitus was an autoimmune disease. Further analyses by Gepts and LaCompte (3) suggested that the islet inflammatory lesion in patients with short duration had surprising features of chronic rather than acute inflammatory appearance. Later, quantitative analyses showed that the loss of β-cells were substantial not only in the pancreas of long-term but also in patients with short-term diabetes (4,5).

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Lernmark, Å., Chung, C.H. (2003). Molecular Biology of β-Cell Destruction by Autoimmune Processes. In: Sperling, M.A. (eds) Type 1 Diabetes. Contemporary Endocrinology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-310-1_4

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