Abstract
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.
Highlights
Type 1 diabetes mellitus results from a loss of insulinproducing β-cells in the pancreatic islets caused by an immune-mediated chronic destructive process
The observed increase of IL-5 secretion in the presence of insulin B9-23 is suggestive of a modulation of the immune response towards a protective Th2 response against islet antigens
Numbers of patients treated with NBI-6024 are still small, these results are encouraging with respect to the ongoing phase II trial in newly diagnosed patients with type 1 diabetes aiming to preserve residual C-peptide
Summary
Type 1 diabetes mellitus results from a loss of insulinproducing β-cells in the pancreatic islets caused by an immune-mediated chronic destructive process. In human type 1 diabetes, new strategies are currently being developed with the aim of actively suppressing the autoimmune process and inducing a lasting tolerance against islet antigens. Modulation of the immune response in newly diagnosed patients with type 1 diabetes through NBI-6024, an altered peptide-ligand of the immunodominant insulin epitope B9-23. NBI-6024 treated adult patients with newly diagnosed type 1 diabetes more often had a B9-23 stimulated IFN-γ secretion (31%). This IFN-γ response could be fully suppressed by increasing the dosage of NBI-6024
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