Modulating the Autoimmune Response in Type 1 Diabetes: A Report on the 64th Scientific Sessions of the ADA, June 2004, Orlando, FL, USA

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The Review of Diabetic Studies,2004,1,3,137-140.
Published:November 2004
Type:Conference Report
Author(s) affiliations:

Peter Achenbach and Martin Füchtenbusch

Diabetes Research Institute, Kölner Platz 1, 80804 Munich, Germany.


Type 1 diabetes mellitus results from a loss of insulinproducing β-cells in the pancreatic islets caused by an immune- mediated chronic destructive process. It is generally believed that immune tolerance to β-cells is broken by environmental factors in genetically susceptible individuals, leading to β-cell destruction that is mediated by T lymphocytes. A key assumption in the current pathogenic concept of type 1 diabetes is a defective immunoregulation affecting both central and peripheral mechanisms of tolerance induction against β-cell antigens. In animal models of type 1 diabetes, disease-protective modulation of the islet autoimmune response can be effected by various strategies including administration of islet antigens. In human type 1 diabetes, therefore, new strategies are currently being developed with the aim of actively suppressing the autoimmune process and inducing a lasting tolerance against islet antigens. In this context, inducing regulatory T cells in vivo (i.e. CD4+CD25+ T cells or type 1 regulatory T cells) is currently becoming more widespread. The following report highlights some of the recent studies on immunotherapy of type 1 diabetes, presented at the 64th Scientific Sessions, held in June 2004, in Orlando, Florida.