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Cell-Mediated Anti-Islet—Cell Immune Response: Clinical Experience and Lessons from Animal Models

  • Chapter
Autoimmunity and the Pathogenesis of Diabetes

Part of the book series: Endocrinology and Metabolism ((EAM,volume 4))

Abstract

The hypothesis that type I, insulin-dependent diabetes mellitus (IDDM) results, at least in part, from the autoimmune destruction of pancreatic beta-cells has been discussed in several reviews,1–3 as well as in other chapters in this volume. Relatively early in the analysis of autoimmunity and diabetes, a small number of papers presented evidence of a direct anti-beta—cell (or pancreatic islet-cell) cellular immune response in individuals with diabetes. It has become clear over the last decade, however, that the results of such studies in humans are limited, at least to the extent that they may be considered beta-cell—specific, by the so-called major histocompatibility complex (MHC)-restriction of the cell-mediated arm of the immune system. The specific effector cell, typically a thymus-derived cell, the T-cell, and the target cell must share identity at one of the class I (cytotoxic/suppressor cells, CD8+) or class II (helper/inducer cells CD4+). This issue of MHC-restriction in the immune system has been reviewed recently.4–5 Although MHC-restriction is not now considered to be an absolute requirement for cell-mediated cytolysis, further research in the description and analysis of the role of the cell-mediated immune response in human diabetes has virtually stopped because of the lack of a biologically relevant, MHC-restricted beta-cell for use as a target. Fortunately studies of the cell-mediated immune response against pancreatic beta-cells are possible in experimental models of diabetes using both in vitro and in vivo techniques.

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McEvoy, R.C., Thomas, N.M. (1990). Cell-Mediated Anti-Islet—Cell Immune Response: Clinical Experience and Lessons from Animal Models. In: Ginsberg-Fellner, F., McEvoy, R.C. (eds) Autoimmunity and the Pathogenesis of Diabetes. Endocrinology and Metabolism, vol 4. Springer, New York, NY. https://doi.org/10.1007/978-1-4612-3218-6_8

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  • DOI: https://doi.org/10.1007/978-1-4612-3218-6_8

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4612-7920-4

  • Online ISBN: 978-1-4612-3218-6

  • eBook Packages: Springer Book Archive

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