Immunogenetics of type 1 diabetes and its associated complications

Mohamed Jahromi

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


Diabetes is one of the fastest growing diseases. World health organization (WHO) estimates that approximately180 million people have diabetes and this number will be doubled by 2030. Type 1 diabetes is an autoimmune disease that is caused as a result of destruction of pancreatic ß-cells. Several factors may contribute to the pathogenesis of type 1 diabetes. Genetic susceptibility of type 1 diabetes is determined by polymorphisms/mutations in multiple genes in both human and animal models. The MHC accounts for approximately 50% of the familial aggregation of type 1 diabetes and the insulin gene for only 10 % suggesting the existence of additional loci. The gene for PTPN22, the lymphocyte signaling molecule, on chromosome 1p13.3-p13.1 is a confirmed locus that contributes to multiple autoimmune disorders, including type 1 diabetes. Diabetes associated CTLA-4 locus polymorphisms in most populations have relative risks less than 1.5. A fundamental question is whether there are genetic polymorphisms that confer major risk for type 1 diabetes, other than the HLA DR and DQ alleles (class II HLA alleles). Recently, genes outside MHC region have considered playing an important role in the onset of diabetes. Environmental factors appear to play an important role in the pathogenesis of type 1 diabetes. The most important factors are thought to be infectious, dietary, and hygienic factor. Enteroviruses , breastfeeding, the early presence or lack of certain foods, birth weight, childhood overnutrition, maternal islet autoimmunity, and negative stress events as well as hygienic factor have been shown to be related to the prevalence of type 1 diabetes.

Original languageEnglish
Title of host publicationType 1 Diabetes
Subtitle of host publicationCauses, Treatment and Potential Complications
Number of pages33
ISBN (Electronic)9781631170010
Publication statusPublished - 1 Jan 2014


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