Abstract
This comprehensive literature review examines the immunopathogenesis of Hashimoto's thyroiditis, a prevalent autoimmune thyroid disorder. Hashimoto's thyroiditis results from a complex interplay of genetic predisposition and environmental triggers, leading to loss of immune tolerance to thyroid antigens. Hashimoto's thyroiditis involves both cellular (T cells) and humoral (B cells, autoantibodies) responses. Key players include Th1, Th17, and regulatory T cells, with an imbalance in the Th17/Treg ratio implicated. The diagnosis of Hashimoto's thyroiditis relies on clinical presentation, thyroid function tests, detection of anti-thyroid peroxidase and anti-thyroglobulin antibodies, and ultrasound imaging. Current treatment of Hashimoto's thyroiditis primarily involves levothyroxine replacement therapy. Emerging adjunctive approaches include vitamin D and selenium supplementation. Some potential challenges of Hashimoto's thyroiditis include understanding precise disease triggers, developing predictive biomarkers, and addressing persistent symptoms despite biochemical euthyroid. This article highlights recent advances in understanding the pathogenesis of Hashimoto's thyroiditis, particularly the roles of Th17 cells and oxidative stress. It also discusses controversies and knowledge gaps, such as the exact mechanisms that initiate autoimmunity and the factors that influence disease progression. There is a need for personalized treatment strategies and therapies targeting the underlying autoimmune process for better treatment of patients with Hashimoto's Thyroiditis.