Abstract
Insulin-dependent diabetes mellitus (IDDM), or type 1 diabetes, is a chronic and yet incurable disease characterized by autoimmune destruction of pancreatic ß-cells and complete insulin deficiency (1). The disease develops predominantly in children or adolescents, but it can develop at a much later age, and it is quite heterogeneous in its clinical expression. A large body of evidence indicates that inherited genetic factors influence both susceptibility to and resistance from the disease. During the past few years, dramatic improvements in the ability to investigate the genetics of complex diseases have been introduced. The increasing availability of polymorphic microsatellite markers, automated typing technology (2), and large collections of families with affected sib-pairs have enabled the design of large scale, genome-wide scans to map IDDM susceptibility genes. Such scans have provided evidence to link diabetes susceptibility with numerous chromosomal regions and suggested that type 1 diabetes is a polygenic disorder. Moreover, there is evidence for epistatic phenomena involving several loci, and complex parental effects appear to influence susceptibility by modifying the transmission and expression of inherited genes.