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 I2 (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, I2 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 ºC 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<0.02), while it did
not affect the level of other cytokines. On the other hand, I2 significantly decreased the level of IL-4 and IL-
10 (P<0.01). In the presence of LPS/PHA, NaI also reduced the production of IL-10 (P<0.02), while I2
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 I2 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.