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- W2915641459 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." @default.
- W2915641459 created "2019-03-02" @default.
- W2915641459 creator A5039395009 @default.
- W2915641459 creator A5080976346 @default.
- W2915641459 date "2017-08-22" @default.
- W2915641459 modified "2023-10-16" @default.
- W2915641459 title "The Genetic Architecture of Type 1 Diabetes" @default.
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- W2915641459 doi "https://doi.org/10.3390/genes8080209" @default.
- W2915641459 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5575672" @default.
- W2915641459 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/28829396" @default.
- W2915641459 hasPublicationYear "2017" @default.
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