Type 1 Diabetes

T1D constitutes <10% of the ~21 million known cases of diabetes in the United States. The disease is characterized by an absolute deficiency of insulin caused by an autoimmune attack on the islet β cells of the pancreas. In T1D, the islets of Langerhans become infiltrated with activated T lymphocytes, leading to a condition called insulitis. Over a period of years, this autoimmune attack on the β cells leads to gradual depletion of the β-cell population (Fig. 1). However, symptoms appear abruptly when 80%–90% of the β cells have been destroyed.
At this point, the pancreas fails to respond adequately to ingestion of glucose, and insulin therapy is required to restore metabolic control and prevent lifethreatening ketoacidosis. β-Cell destruction requires both a stimulus from the environment (such as a viral infection) and a genetic determinant that causes the β cells to be mistakenly identified as “nonself.” [Note: Among monozygotic (identical) twins, if one sibling develops T1D, the other twin has only a 30%–50% chance of developing the disease. This contrasts with T2D , in which the genetic influence is stronger and, in virtually all monozygotic twinships, the disease eventually develops in both individuals.]

Figure 1: Insulin secretory capacity during onset of type 1 diabetes. [Note: Rate of autoimmune destruction of β cells may be faster or slower than shown.]

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