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Activation of cell-mediated immunity by soluble interleukin-2 receptor alpha (sIL-2R α) release is well documented. The aim of this study was to measure serum concentrations of sIL-2R α in patients with autoimmune and non-autoimmune thyroid disorders in different stages of thyroid function, before and after administration of l-thyroxine ( l-T4) and its discontinuation as well as before and during methimazole administration. The study included 80 females: 16 with Graves’ disease, 15 with Hashimoto's thyroiditis and subclinical hypothyroidism, 14 with Hashimoto's thyroiditis with fibrosis and clinical hypothyroidism, 20 after subtotal thyroidectomy following nodular non-toxic goitre and 15 healthy controls. Patients were examined at two different time points. Serum concentrations of sIL-2R α were measured with the use of enzyme immunoassay technique. Souble IL-2R α serum concentration increased in patients with untreated Graves’ disease and decreased after methimazole treatment. In Hashimoto's thyroiditis, the sIL-2R α level was within the normal range, in Hashimoto's thyroiditis with clinical hypothyreosis it was low and after l-T4 administration it increased in both patient groups. After thyroidectomy, patients treated with l-T4, had increased levels of sIL-2R α which decreased after discontinuation of therapy. There were a significant positive correlation between sIL-2R α and free thyroxine in patients with (i) Graves’ disease both before and after methimazole administration, (ii) Hashimoto's thyroiditis (with subclinical hypothyroidism) both before and after l-T4 therapy, (iii) Hashimoto's thyroiditis with fibrosis and (iv) overt hypothyroidism before l-T4 administration and in individuals during long-term l-T4 treatment (after subtotal thyroidectomy). Serum sIL-2R α concentration in autoimmune thyroid diseases depends on thyroid function. In both autoimmune and non-autoimmune thyroid diseases, thyroxine stimulates the release of sIL-2R α. [ABSTRACT FROM AUTHOR]