ABSTRACT
Autoimmune thyroid disease encompasses a spectrum from overt hypothyroidism and/or thyroid inflammation in Hashimoto’s disease to hyperthyroidism in Graves disease. The breakdown in tolerance in these diseases is characterized by the production of autoantibodies, predominantly of IgG class, to thyroid specific proteins: Thyroid peroxidase (TPO, formerly known as the “microsomal antigen”), thyroglobulin (Tg), the thyrotropin receptor (TSHR) and the sodium/iodide symporter (Figure 1). Some individuals have autoantibodies to all four autoantigens. However, thyroid infiltration and thyroid damage in Hashimoto’s thyroiditis is mainly associated with autoantibodies to TPO and Tg (rev. in 1) On the other hand. TSHR autoantibodies that stimulate the thyroid gland are responsible for Graves’ hyperthyroidism (rev. in 2). A small proportion of patients are hypothyroid due to TSHR autoantibodies that block the stimulatory effects of TSH (2).
