New therapies aimed at the preservation or restoration of beta cell function in type 1 diabetes.
Type 1 diabetes is caused by an immune-mediated destruction of the insulin-secreting beta cells in the pancreas. The disease can become clinically apparent at any age. At diagnosis, there is invariably some residual beta cell function and more so in adults than in children. Recent studies--including one conducted mainly in Belgium--have provided proof of principle that short-term anti-T-cell antibody treatment is able to preserve residual beta cell function for at least 18 months. The resultant stabilizing effect on metabolic control is expected to delay or limit chronic complications in these patients. With a similar goal in mind, nonuremic C-peptide negative patients are offered beta cell transplantation. The outcome of these implants looks promising but their final applicability hinges on finding ways to induce immune tolerance to the donor beta cells. A widespread application, however, will only occur if the shortage of viable human donor cells can be overcome. Both xenotransplantation and stem cell therapy provide possible strategies to solve this problem and represent areas of intense investigation. The ultimate goal is prevention of clinical disease. Studies by the Belgian Diabetes Registry and others in first degree family members of type 1 diabetic patients have refined the identification of individuals at very high risk of hyperglycaemia so that new immunological treatments can be tested in the prediabetic phase.
Keymeulen
B
B
Academisch Ziekenhuis and Diabetes Research Centre -Brussels Free University-VUB, Laarbeeklaan 103, B-1090 Brussels, Belgium. Bart.Keymeulen@az.vub.ac.be
D000818:Animals; D000911:Antibodies, Monoclonal / Q000276:immunology; D002096:C-Peptide / Q000097:blood; D017252:CD3 Complex / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000276:immunology / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy*; D018450:Disease Progression; D006031:Glycosylation; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology; D007141:Immunoglobulin Fc Fragments / Q000276:immunology; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D050417:Insulin-Secreting Cells / Q000502:physiology; D016381:Islets of Langerhans Transplantation; D016853:Muromonab-CD3 / Q000627:therapeutic use; D010186:Pancreatic Function Tests; D013601:T-Lymphocytes / Q000276:immunology
D000911:Antibodies, Monoclonal; D002096:C-Peptide; D017252:CD3 Complex; D007141:Immunoglobulin Fc Fragments; D007166:Immunosuppressive Agents; D016853:Muromonab-CD3