The Role of Iodine and Selenium in Autoimmune Thyroiditis

Abstract

AbstractIodine and selenium (Se) are both essential elements to thyroid hormone economy, while they represent key players in the development of autoimmune thyroiditis.Chronic high iodine intake has been associated in various studies with increased frequency of autoimmune thyroiditis. In susceptible individuals, iodine excess increases intra-thyroid infiltrating Th17 cells and inhibits T regulatory (TREG) cells development, while it triggers an abnormal expression of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in thyrocytes, thus inducing apoptosis and parenchymal destruction. As was shown in a mouse model, high iodine supply leads to changes in the immunogenicity of the thyroglobulin molecule, upregulation of vascular intercellular adhesion molecule-1 (ICAM-1), and reactive oxygen species (ROS) generation in the thyrocytes. Serum Se levels were found decreased in Hashimoto thyroiditis and especially in Graves’ disease as well as in thyroid-associated ophthalmopathy patients, the levels being related to the pathogenesis and outcome. Selenium is strongly involved, via the variable selenoproteins, in antioxidant, redox, and anti-inflammatory processes. Selenium enhances CD4+/CD25 FOXP3 and T regulatory cells activity while suppressing cytokine secretion, thus preventing apoptosis of the follicular cells and providing protection from thyroiditis. Selenium supplementation may be useful in autoimmune thyroid diseases, though, while usually well-tolerated, it should not be universally recommended, and it is also likely to be helpful for those with low Se status and autoimmunity. Broadly speaking, the achievement and maintenance of “selenostasis” as well as adequate urinary iodine excretion are mandatory to control disease, while, putatively, they may additionally be critical to preventing disease.