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Genes 2017, 8(8), 209; doi:10.3390/genes8080209

The Genetic Architecture of Type 1 Diabetes

Bart’s and the London School of Medicine and Dentistry, QMUL, London E1 2AT, UK
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Academic Editor: Josyf Mychaleckyj
Received: 12 May 2017 / Revised: 7 August 2017 / Accepted: 16 August 2017 / Published: 22 August 2017
(This article belongs to the Special Issue Genetics and Functional Genomics of Diabetes Mellitus)
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Abstract

Type 1 diabetes (T1D) is classically characterised by the clinical need for insulin, the presence of disease-associated serum autoantibodies, and an onset in childhood. The disease, as with other autoimmune diseases, is due to the interaction of genetic and non-genetic effects, which induce a destructive process damaging insulin-secreting cells. In this review, we focus on the nature of this interaction, and how our understanding of that gene–environment interaction has changed our understanding of the nature of the disease. We discuss the early onset of the disease, the development of distinct immunogenotypes, and the declining heritability with increasing age at diagnosis. Whilst Human Leukocyte Antigens (HLA) have a major role in causing T1D, we note that some of these HLA genes have a protective role, especially in children, whilst other non-HLA genes are also important. In adult-onset T1D, the disease is often not insulin-dependent at diagnosis, and has a dissimilar immunogenotype with reduced genetic predisposition. Finally, we discuss the putative nature of the non-genetic factors and how they might interact with genetic susceptibility, including preliminary studies of the epigenome associated with T1D. View Full-Text
Keywords: Type 1; diabetes; genetic; genes Type 1; diabetes; genetic; genes
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Jerram, S.T.; Leslie, R.D. The Genetic Architecture of Type 1 Diabetes. Genes 2017, 8, 209.

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