Modulating the autoimmune response in type 1 diabetes: a report on the 64th scientific sessions of the ADA, June 2004, Orlando, FL, USA.
Type 1 diabetes mellitus results from a loss of insulin-producing beta-cells in the pancreatic islets caused by an immune-mediated chronic destructive process. It is generally believed that immune tolerance to beta-cells is broken by environmental factors in genetically susceptible individuals, leading to beta-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 beta-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.
Achenbach
Peter
P
Diabetes Research Institute, Kölner Platz 1, 80804 Munich, Germany.
Füchtenbusch
Martin
M