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• W3174557356 abstract "Life is about timing. —Carl Lewis The understanding of autoimmune type 1 diabetes is increasing, and examining etiology separate from pathogenesis has become crucial. The components to explain type 1 diabetes development have been known for some time. The strong association with HLA has been researched for nearly 50 years. Genome-wide association studies added another 60+ non-HLA genetic factors with minor contribution to risk. Insulitis has long been known to be present close to clinical diagnosis. T and B cells recognizing β-cell autoantigens are detectable prior to diagnosis and in newly diagnosed patients. Islet autoantibody tests against four major autoantigens have been standardized and used as biomarkers of islet autoimmunity. However, to clarify the etiology would require attention to time. Etiology may be defined as the cause of a disease (i.e., type 1 diabetes) or abnormal condition (i.e., islet autoimmunity). Timing is everything, as neither the prodrome of islet autoimmunity nor the clinical onset of type 1 diabetes tells us much about the etiology. Rather, the islet autoantibody that appears first and persists would mark the diagnosis of an autoimmune islet disease (AID). Events after the diagnosis of AID would represent the pathogenesis. Several islet autoantibodies without (stage 1) or with impaired glucose tolerance (stage 2) or with symptoms (stage 3) would define the pathogenesis culminating in clinical type 1 diabetes. Etiology would be about the timing of events that take place before the first-appearing islet autoantibody." @default.
• W3174557356 created "2021-07-05" @default.
• W3174557356 creator A5008841181 @default.
• W3174557356 date "2021-07-01" @default.
• W3174557356 modified "2023-09-23" @default.
• W3174557356 title "Etiology of Autoimmune Islet Disease: Timing Is Everything" @default.
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• W3174557356 doi "https://doi.org/10.2337/dbi18-0034" @default.
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