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Islet autoantibodies have taught us almost all we knowabout the disease process leading up to type 1 di-abetes (T1D). In the absence of direct access to targetorgan tissue prior to diagnosis, they have provided the best available window on islet autoimmunity in humans. Detection of islet cell antibodies (ICA) in unaffected rela-tives identified for the first time the prodrome preceding clinical onset (1), and autoantibodies to insulin (IAA), glu-tamate decarboxylase (GADA), islet antigen-2, and zinc transporter 8 now provide the foundations for studies of the natural history of the condition. In prospective studies from birth, such as Diabetes Autoimmunity Study of the Young (DAISY), BABYDIAB, Diabetes Prediction and Prevention (DIPP), and more recently The Environmental Deter-minants of Diabetes in the Young (TEDDY), appearance of islet autoantibodies has been used to define the onset of autoimmunity (2–5). This can then be related to ge-netic characteristics and environmental exposures of
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Bingley et al. (2013) studied this question.
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