Research on the Mechanism of T Cell Subsets and Cytokines in Hashimoto's Thyroiditis

Abstract

As being one of the most common diseases in autoimmune thyroid disease (AITD), Hashimoto's thyroiditis (HT) is an organ-specific autoimmune disease. It is mostly related to genetics, infection, and excessive iodine, but the exact pathogenesis has not yet clear. As one of the most important immune cells, T cells play an important role in the human immune. Helper T cells (Th) and regulatory T cells (Treg) are two important subgroups of T cells. The former include Th1, Th2, Th17 and other cells. HT patients is mainly characterized by expressing Th1 cytokines. The imbalance of Th1/Th2 ratio can induce abnormal immune response, which is closely related to the incidence of HT. Th17/Treg cells are mutually restricted in differentiation and mutually antagonistic in function. IL-17 secreted by Th17 cells directly promotes the inflammatory response of thyroid tissue and accelerates the damage of thyroid tissue. Abnormal Treg cell function cannot effectively inhibit the occurrence of autoimmune reactions and promote immune tolerance. Th17/Treg constitute a relatively independent group of cell networks except Th1/Th2. Under normal circumstances, Th1/Th2 and Th17/Treg cells maintain a dynamic balance. However, once unbalanced, they will lead to immune dysfunction and participate in the development of HT. This article reviews the mechanisms of Th1/Th2 and Th17/Treg cells and their cytokines in the pathogenesis of HT.