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Background:  IL-36α is involved in the pathogenesis of a variety of autoimmune diseases, but the relationship between IL-36α and Graves' disease (GD) has rarely investigated. In the present study, we aimed to explore the expression of IL-36α and elucidate the potential role of IL-36α in GD.   Methods:  The expression of IL-36α mRNA in peripheral blood mononuclear cells (PBMCs) from 32 newly diagnosed GD patients, 15 refractory GD patients and 30 normal controls (NC) was examined using quantitative real-time polymerase chain reaction (qRT-PCR). The level of IL-36α in serum from 46 newly diagnosed GD patients, 10 refractory GD patients and 24 NC was measured using enzyme linked immunosorbent assay (ELISA). The percentage of CD4 + IL-36α + T cells was detected by flow cytometry. PBMCs from newly diagnosed GD patients and NC group were cultured in the presence or absence of recombinant human IL-36α, and the expression levels of IFN-γ, TNF-α, IL-6, and IL-17A in culture supernatant were detected by cytokine array.   Results:  The expression of IL-36α mRNA in newly diagnosed GD patients was significantly higher than that in NC group ( P  = 0.019). IL-36α mRNA expression was positively associated with thyrotropin receptor antibody (TRAb) ( P  = 0.004,  r  = 0.498) in newly diagnosed GD patients. The level of IL-36α in serum from newly diagnosed GD patients was significantly higher than that in refractory GD patients and NC group ( P  = 0.01;  P  = 0.007). The percentage of CD4 + IL-36α + T cells in newly diagnosed GD patients was significantly higher than that in NC group ( P  = 0.030). In GD group, recombinant human IL-36α stimulation resulted in the increase of INF-γ, TNF-α, IL-6 and IL-17A ( P  = 0.015;  P  = 0.016;  P  = 0.039;  P  = 0.017).   Conclusion:  IL-36α and CD4 + IL-36α + T cells may be involved in the pathogenesis of GD by promoting the production of Th1, Th2, and Th17 cytokines.

Elevated Interleukin-36α And CD4+IL-36α+T Cells Are Involved in the Pathogenesis of Graves' Disease