The aim: Autoimmune thyroid disease (AITD) is the organ specific autoimmune disorder. It comprises two major clinical entities: Graves’ disease and Hashimoto's thyroiditis, both characterised by the presence of thyroid specific autoantibodies directed against three major thyroid antigens: TSH receptor, thyroid peroxidase and thyroglobulin. It has been established that the proinflammatory, T helper cell 1 (Th1) type and Th1 cytokines play the major role in the pathogenesis of organ specific autoimmune diseases while the protective role goes to T helper cell 2 (Th2) type and Th2 cytokines. Normal pregnancy is characterised by Th2 domination over Th1 immunity which explains the amelioration of autoimmune disorders. However, after delivery, the Th1/Th2 ratio changes and exacerbation of autoimmune disorders usually occurs. If AITD is induced by Th1 mechanisms, the Th2/Th1 switch could explain the aggravation of AITD after delivery. Still, the exact patophysiological mechanism remains unclear. NKT and regulatory T cells are considered to have a central role in prevention of autoimmunity and maintaining tolerance of allogenic transplants. The alterations of immunological parameters during AITD remain unclear, especially those concerning AITD during pregnancy. Our aim was to investigate the influence of the immunological parameters during pregnancy and in the postpartum on the development of AITD, more precisely the influence of Th, NK, NKT and T regulatory cells, to correlate the results with the hormone levels and to compare them with healthy pregnant and non pregnant women. Patients and Methods: We investigated the presence of AITD in women during pregnancy and after delivery by analysing the thyroid hormone levels, thyroid antibody titres and ultrasound examination. We compared the results with healthy pregnant and postpartum VIII women and non pregnant controls. The phenotype and cytolytic potential of peripheral blood mononuclear cells of non pregnant, pregnant and postpartum women was analysed by flow cytometry after intracellular and surface staining. Results: The mean TSH level gradually increases during pregnancy, although not significantly compared to non pregnant women. It falls in the postpartum and is significantly lower compared to the second half of pregnancy. The mean FT4 level decreases during pregnancy and is significantly lower compared to non pregnant women, while in the postpartum it is significantly higher than during pregnancy. Positive autoantibodieas were found in 16% of euthyroid pregnant and 24% of euthyroid postpartum women. The mean TSH level in euthyroid pregnant women with positive antibodies was slightly, but not significantly, higher compared to control pregnancy. Subclinical or overt hypothyroidism was diagnosed in 8,6 % of pregnant and 14% of postpartum women while 2, 7 % of pregnant and 2,6% of postpartum women were in subclinical or overt hyperthyroidism. Postpartum thyroiditis was diagnosed in 6,5% of women. Thyroid autoimmunity was found in 25% of pregnant and 41,5 % of postpartum women. The cells of innate immunity: NKT and Tregs were elevated in healthy pregnancies and in pregnancies with hypo-and hyperthyroidism, as well as postpartum in all experimental groups. NKT cells were reduced in pregnant women with positive antibodies indicating a decrease in NKT cell protective effect of pregnancy under the action of antibodies. Total perforin was decreased in healthy pregnancy, but higher in patients with positive antibodies, hypo-and hyperthyroidism and postpartum indicating the increased cytolytic potential of these cells in autoimmune process. Conclusion: The pregnancy and postpartum influence the course of AITD, while thyroid autoimmunity also has an impact on the thyroid function during gestation and in the early postpartum. Both, NKT and T reg cells play an important role in regulation of autoimmunity in pregnant and postpartum women with AITD.