Pathogenic Mechanisms of Autoimmune Thyroid Disease

Abstract

Autoimmune thyroid illnesses are a category of disorders characterized by aberrant lymphocyte activity directed against self-tissues and are mostly represented by Hashimoto's thyroiditis and Graves' disease, which affect about 2% to 3% of the population, with a female predominance. Autoimmune thyroid disease is the most prevalent thyroid illness in children; the most typical age of onset is puberty, although the disease can strike at any age, including children as young as one-year-old. Autoantibodies to pendrin, an iodide transporter found at the apical pole of thyroid follicular cells, have recently been discovered in the majority of Hashimoto's thyroiditis and Graves' disease patients. Excessive iodine administration has been linked to an increased prevalence of thyroiditis in humans, according to recent epidemiologic research. People in North America consumed more than three times the recommended daily iodine intake. Antithyroglobulin antibody, anti-thyroperoxidase antibody, serum thyroid-stimulating hormone, and exacerbation of lymphocytic infiltration in the thyroid were all higher in these persons, indicating that iodine overconsumption could cause hypothyroidism and exacerbate the autoimmune response. However, the exact mechanism by which high iodine consumption causes autoimmune thyroid disease is yet unknown.