"In GD, proinflammatory cytokines such as IL-6 may further induce the synthesis of external thyroid-stimulating antibodies that bind to TSHR. [74] IFN?? can also contribute to an autoimmune inflammatory response via a variety of mechanisms, such as reducing T regulatory cell function and alterations in immunoglobulin production. [75],[76] Th1 polarization may constitute a potentially important ther" . . . .