Type 1 diabetes (T1D) occurs in individuals with a genetic predisposition to the disease, predominantly from a human leukocyte antigen (HLA)-related immunogenotype that accounts for approximately 60% of the genetic influence. In these individuals who are genetically at risk, an environmental trigger is thought to initiate an immune response targeting the insulin-secreting pancreatic islet β cells.1,2 The initial immune response also may engender secondary and tertiary immune responses that contribute to the impairment of β-cell function and destruction of β cells.3 The rate of development of T1D varies, probably related to non-HLA genetic factors and additional environmental factors beyond the triggering exposure.4
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