HLA and diabetes.
HLA studies have conclusively demonstrated that IDDM and non-IDDM are separate disease entities. A considerable part of the genetic susceptibility to IDDM is due to one or more HLA genes. The HLA-DR3 and -DR4 factors showing the strongest association with IDDM belong to the so-called DR antigens, which are believed to be the immune response determinants of man. A dominant model for the HLA-controlled susceptibility to IDDM has been ruled out and a recessive model seems unlikely. A gene-dose model intermediate between dominance and recessivity is still possible, but there is also some evidence against this model, because DR3/4 heterozygotes seem to have a considerably higher risk of developing IDDM than has DR3/3 and DR4/4 homozygotes. It has been suggested that DR3 (or a DR3-associated factor) and DR4 (or a DR4-associated factor) confer susceptibility to IDDM each by a separate mechanism, and more recently that DR3/4 heterozygotes may carry combinatorial antigens which could contribute to the susceptibility to IDDM. Studies of HLA-associated clinical heterogeneity within IDDM are indicated to gain further insight in the genetics of IDDM.
D003920:Diabetes Mellitus / Q000188:drug therapy / Q000235:genetics / Q000276:immunology*; D005006:Ethnicity; D005787:Gene Frequency; D005799:Genes, Dominant; D005808:Genes, Recessive; D006680:HLA Antigens / Q000235:genetics*; D006801:Humans; D007328:Insulin / Q000627:therapeutic use; D008957:Models, Genetic; D044469:Racial Groups
D006680:HLA Antigens; D007328:Insulin