Conference Reports

Rev Diabet Stud, 2004, 1(3):137-140

DOI 10.1900/RDS.2004.1.137

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

Peter Achenbach, Martin Füchtenbusch

Diabetes Research Institute, Kölner Platz 1, 80804 Munich, Germany.
Address correspondence to: Martin Füchtenbusch, e-mail: martin.fuechtenbusch@lrz.uni-muenchen.de

Abstract

Type 1 diabetes mellitus results from a loss of insulin-producing 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 64^th Scientific Sessions, held in June 2004, in Orlando, Florida.

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Rev Diabet Stud, 2004, 1(3):141-144

DOI 10.1900/RDS.2004.1.141

Type 1 Diabetes and NKT Cells: A Report on the 3rd International Workshop on NKT Cells and CD1-Mediated Antigen Presentation, September 2004, Heron Island, QLD, Australia

Julie M. Fletcher, Margaret A. Jordan, Alan G. Baxter

Comparative Genomics Centre, Molecular Sciences Building 21, James Cook University, Townsville QLD 4811, Australia.
Address correspondence to: Alan G. Baxter, e-mail: alan.baxter@jcu.edu.au

Abstract

NKT cells play a major role in regulating the vigor and character of a broad range of immune responses. Defects in NKT cell numbers and function have been associated with type 1 diabetes, especially in the NOD mouse model. The 3rd International Workshop on NKT Cells and CD1-Mediated Antigen Presentation provided an opportunity for researchers in the field of NKT cell biology to discuss their latest results, many of which have direct relevance to understanding the etiology and pathogenesis of diabetes.

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