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This article is part of the supplement: 25th European Workshop for Rheumatology Research

Oral presentation

Autoimmune diabetes: mechanisms

A Cooke

  • Correspondence: A Cooke

Author affiliations

University of Cambridge, UK

Citation and License

Arthritis Research & Therapy 2005, 7(Suppl 1):S3  doi:10.1186/ar1508

The electronic version of this article is the complete one and can be found online at:


Received:11 January 2005
Published:17 February 2005

© 2005 BioMed Central Ltd

Oral presentation

Type 1 diabetes is an autoimmune disease that is increasing dramatically in incidence in the developed world. Explanations for this increase in incidence include viral precipitation of disease and the so-called 'hygiene hypothesis'.

In Type 1 diabetes the insulin-producing beta cells of the pancreas are selectively destroyed by the immune system. Type 1 diabetes is generally recognised as a T-cell-mediated autoimmune disease with the autoantibody response to islet antigens serving as markers of ongoing beta cell destruction.

Studies in spontaneous animal models of this human condition suggest that it is a Th1-mediated autoimmune disease with an involvement of both CD8+ T cells and macrophages in pathology. There are multiple ways in which the beta cell could be destroyed including a Class I restricted killing by CD8+ T cells, proinflammatory cytokine-mediated cell death and death induced by Fas/FasL interactions.

At the time of clinical diagnosis it is possible that the patient will have destroyed 70% of their beta cell mass and exogenous insulin is required to maintain glucose homeostasis. There is currently much interest in the development of tolerogenic strategies to inhibit and halt beta destruction. This coupled with strategies to facilitate the replacement of the destroyed beta cells would constitute a cure for this disease.