There is increasing evidence showing that apoptosis plays a role in the development of the autoimmune thyroid diseases-Hashimoto's (lymphocytic) thyroiditis (HT) and Graves' disease (GD). The immune pathogenesis of HT and GD is not yet fully understood, but evidence points toward several steps. A defect in CD4(+)CD25(+) T regulatory cells breaks the immunological tolerance of the host and induces an abnormal production of cytokines, which facilitates the initiation of apoptosis. Though apoptosis appears to play a role in the pathogenesis of both HT and GD, the mechanisms that mediate these processes appear different. The induction of apoptosis in HT results in the destruction of thyrocytes, while apoptosis in the GD leads to damage of thyroid-infiltrating lymphocytes. The differences in the apoptotic mechanisms produce two very different forms of thyroid autoimmune responses, eventually developing into HT and GD, respectively.