Autoimmune
thyroid diseases (AITD) are one of the most common organ-specific autoimmune disorders, of which Hashimoto's
thyroiditis (HT) and
Graves' disease (GD) are 2 of the most common clinical expressions. HT is characterized by
hypothyroidism that results from the destruction of the thyroid by
thyroglobulin-specific T cell-mediated autoimmune response. In contrast, GD is characterized by
hyperthyroidism due to excessive production of
thyroid hormone induced by
thyrotropin receptor-specific stimulatory
autoantibodies.
Cytokines play a crucial role in modulating immune responses that affect the balance between maintenance of self-tolerance and initiation of autoimmunity. However, the role of
cytokines is often confusing and is neither independent nor exclusive of other immune mediators. A regulatory
cytokine may either favor induction of tolerance against thyroid
autoimmune disease or favor activation and/or exacerbation of autoimmune responses. These apparently contradictory functions of a given
cytokine are primarily influenced by the nature of co-signaling delivered by other
cytokines. Consequently, a thorough understanding of the role of a particular
cytokine in the context of a specific immune response is essential for the development of appropriate strategies to modulate
cytokine responses to maintain or restore health. This review provides a summary of recent research pertaining to the role of
cytokines in the pathogenesis of AITD with a particular emphasis on the therapeutic applications of
cytokine modulation.