Introduction: The contribution of Th17 cytokines to autoimmune thyroid disease (AITD) is generally accepted. However, the roles of Th17 cells in the initiation and progression of Hashimoto's thyroiditis (HT) and Graves' disease (GD) remain unclear. Selenium deficiency, along with genetic predisposition and environmental factors, may have a role in thyroid autoimmunity.
Aim: We aimed to assess (1) the Th17 immune response by measuring plasma levels of Th17- and Treg-associated cytokines and (2) the selenium status in treatment-naïve Latvian patients with newly diagnosed GD or HT.
Methods: Eleven GD patients, 41 HT patients, and 26 healthy subjects were recruited for this study. Plasma levels of IL-17a, IL-22, IL-23, IL-6, and IL-10 were detected by xMAP technology, while selenium was detected fluorometrically.
Results and conclusions: No significant differences in IL-17a, IL-22, IL-23, IL-6, or IL-10 levels were found among the HT patients, GD patients, and controls. In the HT patients, IL-17a levels were positively correlated with IL-22, IL-23, IL-6, and IL-10, while IL-22 was correlated with IL-6, IL-23, and IL-10. In the GD patients, IL-17a levels were positively correlated with IL-22, IL-23, and IL-10; IL-22 was positively correlated with IL-23, IL-6, and IL-10; FT3 was positively correlated with IL-17a, IL-23, and IL-10; and FT4 was positively correlated with IL-17a and IL-10 levels. Plasma selenium levels were negatively correlated with antithyroid peroxidase antibody titers in the HT patients. Although no difference in selenium levels was observed between the AITD patients and controls, the selenium status of the Latvian patients with GD or HT was at a suboptimal level.
Keywords: T helper 17 cells; autoimmune thyroid disease; selenium.
© 2021 The Authors. Immunity, Inflammation and Disease published by John Wiley & Sons Ltd.