Recent advances in the immunogenetics of human type 1 diabetes.
Type 1 diabetes (T1D), a disorder of glucose homeostasis, is caused by autoimmune destruction of the essential insulin-secreting beta cells in the pancreas. Both genetic and environmental factors contribute to the risk of T1D and, for decades, this complexity has challenged investigators interested in identifying the genes that contribute to this risk. Nevertheless, in recent years, a number of well-supported T1D risk loci have been identified and replicated. Owing to development of more powerful study designs, the availability of dense marker maps, progress in high-throughput genotyping and a better basic understanding of the roles of genes in the immune system, this trend is likely to continue.
Onengut-Gumuscu
Suna
S
Program in Molecular Genetics, Benaroya Research Institute, Seattle, WA 98101-2795, USA.
Concannon
Patrick
P
D000483:Alleles; D015551:Autoimmunity / Q000235:genetics; D003922:Diabetes Mellitus, Type 1 / Q000201:enzymology / Q000235:genetics* / Q000276:immunology; D006801:Humans; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D054596:Protein Tyrosine Phosphatase, Non-Receptor Type 22; D017027:Protein Tyrosine Phosphatases / Q000235:genetics / Q000276:immunology
C516765:PTPN22 protein, human; D054562:Protein Tyrosine Phosphatase, Non-Receptor Type 1; D054596:Protein Tyrosine Phosphatase, Non-Receptor Type 22; D017027:Protein Tyrosine Phosphatases