COVID‐19‐induced autoimmune thyroiditis: Exploring molecular mechanisms

Abstract Severe acute respiratory syndrome coronavirus‐2 (SARS‐CoV‐2) damages multiple organs, including the thyroid, by direct invasion and cell entry via angiotensin‐converting enzyme 2 or indirectly by promoting excessive inflammation in the body. The immune system is a critical factor in antiviral immunity and disease progression. In the context of SARS‐CoV‐2 infection, the immune system may become overly activated, resulting in a shift from regulatory to effector responses, which may subsequently promote the development and progression of autoimmune diseases. The incidence of autoimmune thyroid diseases, such as subacute thyroiditis, Graves' disease, and Hashimoto's thyroiditis, increases in individuals with COVID‐19 infection. This phenomenon may be attributed to aberrant responses of T‐cell subtypes, the presence of autoantibodies, impaired regulatory cell function, and excessive production of inflammatory cytokines, namely interleukin (IL)‐6, IL‐1β, interferon‐γ, and tumor necrosis factor‐α. Therefore, insights into the immune responses involved in the development of autoimmune thyroid disease according to COVID‐19 can help identify potential therapeutic approaches and guide the development of effective interventions to alleviate patients' symptoms.