[The role of genetic and immunological factors in the etiology of insulin-dependent diabetes]

Abstract

The mechanism of pancreatic B-cell destruction in type I (insulin-dependent) diabetes (IDDM) involves autoimmune phenomena based on genetic predisposition. The mechanism of action of the susceptibility genes is probably related to the function of the HLA molecules in the immune response. The genetic susceptibility is distinguished by increased frequency of the HLA antigens DR3 and DR4 and particularly their heterozygous combination DR3/DR4. Recent advances in molecular biology have resulted in a more precise definition of the genetic variants and corresponding amino acid sequences associated with IDDM. These markers may identify subjects at risk of developing the disease. However, the signs of islet-specific autoimmunity, e.g. islet-cell antibodies, which may be detected several years before the clinical onset of IDDM, are of greater predictive value. These and other arguments in favour of an autoimmune pathogenesis of type I diabetes have made preventive immunotherapy a goal for the future.