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Heat Shock Protein 60 and Type I Diabetes

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Stress Proteins

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 136))

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Abstract

Type I diabetes is characterised by the destruction of pancreatic insulin secreting beta cells and is commonly believed to have an autoimmune aetiology. During the clinically silent, early stages of disease the pancreas is infiltrated by inflammatory cells which mediate beta cell damage. The failure of glucose homeostasis observed in patients is a direct consequence of immunologically mediated beta cell destruction. While there is general agreement that diabetes is caused by autoreactive T cells, there is considerable debate about the antigen specificity of the diabetogenic T cells. As in other autoimmune diseases, identification of the target autoantigen(s) has become a major challenge with potential rewards in new therapies. However, there are no T cell mediated autoimmune diseases in which it has been possible to establish with certainty which self peptides trigger the initial pathology and which major histocompatibility complex (MHC) products present them.

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© 1999 Springer-Verlag Berlin Heidelberg

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Newton, S.G., Altmann, D.M. (1999). Heat Shock Protein 60 and Type I Diabetes. In: Latchman, D.S. (eds) Stress Proteins. Handbook of Experimental Pharmacology, vol 136. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58259-2_16

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  • DOI: https://doi.org/10.1007/978-3-642-58259-2_16

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-63519-9

  • Online ISBN: 978-3-642-58259-2

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