Graves' disease (GD) is a systemic autoimmune syndrome manifesting complications in thyroid and orbital connective tissues. The thyroid gland plays a major role in the human body by producing the hormones necessary for appropriate energy levels and an active life. At the same time, the thyroid is highly vulnerable to autoimmune thyroid diseases. GD arises due to the complex interplay of genetic, environmental and endogenous factors, and the specific combination is required to initiate thyroid autoimmunity. Earlier studies have demonstrated the autoimmune response plays a dominant role in the development of GD. This review summarizes the inflammatory events which occur during the development of GD, such as Th17/Treg cell infiltration, Th1/Th2 cytokine and chemokine production, and the subtypes of immunogloblins (IgGs) generated.