Abstract

Abstract: Background & Aims: While iodine is an essential element for the synthesis of thyroid hormones, epidemiological studies have showed that excessive iodine intake leads to autoimmune thyroid diseases, with an unknown mechanism. Previous studies have showed disturbance in the circulating cytokines could lead to autoimmune diseases. To determine the role of iodine in cytokine production and development of thyroid autoimmune diseases, whole blood was stimulated with NaI (10 mm) and I 2 (0.5 mm). Methods: After evaluation of laboratory results of 25 healthy females (aged 40-45 years), 10 subjects with matched results were selected. Ten ml of sterile heparinized peripheral blood was taken from each subject and immediately were divided into 6 groups (control, NaI stimulated, I 2 stimulated and matching groups in presence of standard stimulators (LPS 1µg/ml & PHA 10µg/ml). Three identical sets were setup to investigate cytokine production at 24, 48, and 72 hours. All samples were incubated in cell culture incubator (95% O2 and 5% CO2) and after elapse of appropriate time, plasma was separated from each well and kept at -70 °C till the time of cytokines (IL-4, IL-10, INF-γ and TGF-β1) analysis. Results: NaI could significantly decrease the production of TGF-β1at all time points (P 2 significantly decreased the level of IL-4 and IL-10 (P 2 decreased the level of IL-4 as well as IL-10 (P<0.01). Conclusion: For the first time, the results of this study indicated that high levels of NaI and I 2 may reduce the level of protective cytokines in circulation. Finally, since neither thyroid hormones nor thyroid gland had role in this process, it may be concluded that thyroid autoimmunity is initiated from high consumption of iodine leading to the imbalance in cytokine production. Keywords: Autoimmune thyroid diseases, High iodine intake, Iodine, Sodium iodide, TGF-β1, INF-γ,

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