LAUSR

Thyroid-associated ophthalmopathy, an ordinary extrathyroid syndrome of Graves' disease (GD), is closely associated with immunity. T helper（Th）17, Th1 and Th2 cells in Th lineages are thought to be related to the disease pathogenesis. Recently, there has been growing evidence that Th17.1 cells are involved in the development and progression of thyroid-associated ophthalmopathy. This pathology is characterized by the presence of Th1 and Th17 lymphocytes, which secrete interferon (IFN)-γ and interleukin (IL)-17A. This paper reviews the potential role of the Th17.1 subgroup pathogenesis of thyroid-associated ophthalmopathy. The therapeutic effects of drugs that can modulate th17.1 cell populations are also highlighted. Rich Th17.1 cells exist in peripheral blood and ocular tissues of patients suffering from thyroid eye disease, especially those with severe or steroid-resistant thyroid-associated ophthalmopathy. The bias of Th17.1 cells to secrete cytokines partly determines the pathological outcome of thyroid-associated ophthalmopathy patients. Th17.1 cells are important in regulating fibrosis, adipocyte differentiation and hyaluronic acid production. In summary, the Th17.1 subpopulation is essential in the onset and progression of thyroid eye disease, and targeting Th17.1 cell therapy may be a promising therapeutic approach.