Graves' disease is the main cause of clinically hyperthyroidism, accounting for about 75% to 80%, and it occurs in women of childbearing age. Clinical manifestations include: high eating, weight loss, sweating, palpitations, emotional excitement and other high metabolism Syndrome. Some patients may have manifestations such as infiltrating exophthalmos and pretibial mucinous edema.

Graves' disease is an organ-specific autoimmune disease characterized by the production of a specific antibody TRAb against thyroid stimulating hormone receptor (TSHR). TRAb can mimic the role of thyroid stimulating hormone, combined with TSHR, stimulating TRAb can cause continuous activation of cAMP, resulting in increased production and release of thyroid hormone. Excessive thyroid hormones in the circulation act on body tissues to cause hypermetabolism and goiter. The pathogenesis of Graves' disease is currently unclear. The three major factors of genetics, environment and immunity are involved in the onset of Graves' disease. There is no doubt that the immune factor is an important factor in the pathogenesis of Graves' disease hyperthyroidism. Studies have shown that CD4+ T cells play an important role in Graves disease. CD4+ T lymphocytes can accept antigens presented by antigen presenting cells, secrete cytokines and assist B lymphocytes to differentiate into plasma cells and produce antibodies. CD4+T accounts for about 40% to 60% of peripheral T cells and can be differentiated into various T cell subsets such as Th1, Th2, Th17, Th22, Th9 and Treg cells. Treg cells are regulatory T cells, mainly involved in the negative regulation of inflammation. Recent researches suggest that the decrease in Treg cell number or loss of function is related to the pathogenesis of various autoimmune diseases. The investigators' previous study showed that the proportion of Treg cells in peripheral blood mononuclear cell of patients with initial Graves' disease was significantly lower than that of healthy controls, and it was negatively correlated with TRAb levels. At the same time, studies have shown that in the early stage of Graves' disease, the number of pDC cells as the main antigen presenting cells has increased. In vitro studies have confirmed that pDC secretes IFN-α to induce differentiation of naive T cells and interferes with the normal immunosuppression of Treg cells. Function, induce apoptosis of Treg cells. Therefore, the weakened immunosuppressive effect of Treg cells also plays a role in the pathogenesis of Graves' disease.

Graves' disease is an autoimmune disease, but the current treatments for Graves' disease: antithyroid drugs, radioactive 131I, surgery, but there is no treatment method through direct immune modulation. Surgery and radioactive 131I treatment achieve rapid cure by removing or damaging the thyroid gland. Surgery is invasive treatment. There are neurovascular injury and anesthesia complications. Most patients with secondary thyroid dysfunction after radioactive 131I treatment require oral L-T4 for life.Compared with the other two methods, antithyroid drug treatment has the advantages of non-invasiveness, convenience, and ease of acceptance by patients, but it has the problems of long treatment duration, low remission rate, and easy recurrence. It also has the induction of agranulocytosis, liver function damage, and rash.

However, there are still few observational follow-up studies on Graves' disease in China, and there are few research reports in this regard.