Interleukins in Graves Disease

The pathogenesis of Graves′ disease, an autoimmune thyroid disorder, remains incompletely understood. Increasing clinical and experimental evidence shows that genetic predisposition, disturbances of the immune system function and environmental factors affecting thyroid gland activity appear to play crucial roles. Graves′ disease is characterized by hyperthyroidism and/or ophthalmopathy related to retroorbital tissue infiltration by autoreactive T-lym-phocytes (1 ). The hallmarks of the disorder, which have been considered to be responsible for ophthalmopathy, hyperthyroidism, acropachy, pretibial derm-opathy, and goiter are factors such as circulating antibodies against thyroid autoantigens (mainly to thyrotropin [TSH] receptor) (2 ,3 ), association with immune response (HLA-DR ) genes (4 –8 ), and an intermittent clinical course of exacerbations and remissions. It has been also proved that in Graves′ disease autoantibodies are capable of stimulating the synthesis of hormones in thyrocytes via the central autoimmune target TSH receptor, which has been cloned and sequenced (9 ). Most patients with Graves′ disease are hyperthoid. The availability of free thriiodothyronin (fT₃ ), free thyroxin (fT₄ ), and highly sensitive TSH techniques has vastly simplified the diagnosis of the early subclinical form of hyperthyroidism (7 ). Development of TSH receptor autoantibody assays (10 ) has enhanced the ability of the clinician to identify subtle presentation of this autoimmune thyroid disease (7 ).