MST-4 and TRAF-6 expression in the peripheral blood mononuclear cells of patients with Graves’ disease and its significance

Background MST-4 and TRAF-6 are involved in the regulation of inflammatory and immune responses. However, whether they participate in the pathogenesis of Graves’ disease (GD) has not yet been reported. Therefore, the purpose of this study was to investigate the expression of MST-4 and TRAF-6 in the peripheral blood of patients with GD to understand their role in the pathogenesis of GD. Methods Thirty newly diagnosed GD patients, 24 GD patients in remission (eGD) and 30 normal controls (NC) were recruited. Thyroid function and autoantibody levels were determined using a chemiluminescence immunoassay. Peripheral blood mononuclear cells (PBMCs) were extracted, and MST-4 and TRAF-6 mRNA and protein levels were determined using real-time PCR and Western blotting, respectively. Results 1. Thyroid function in the GD group was significantly different from that in the eGD and NC groups ( P < 0.05); however, there was no difference in thyroid function between the eGD group and the NC group ( P > 0.05). The autoantibody levels in the NC group were significantly different from those in the GD and eGD groups ( P < 0.05); however, the difference in the levels between the GD group and eGD group was not statistically significant ( P > 0.05). 2. The MST-4 and TRAF-6 mRNA and protein levels in the GD group were significantly lower than those in the NC group ( P < 0.05); however, there were no differences in mRNA and protein levels between the GD group and the eGD group or between the eGD group and the NC group ( P > 0.05). 3. The correlation between the MST-4 and TRAF-6 mRNA and protein levels was not significant. However, there was a significant correlation between the TRAF-6 mRNA and TPO Ab levels in the eGD group and between the TRAF-6 mRNA and TR Ab levels in the NC group. Conclusion The MST-4 and TRAF-6 mRNA and protein levels were lower in the GD group than in the NC group, suggesting that MST-4 and TRAF-6 may be important in the pathogenesis of GD. Whether MST-4 influences the innate immune response through TRAF-6 and thus regulates the imbalance in downstream effector T cells requires further study. Investigating the expression of MST-4 and TRAF-6 in GD can provide a new perspective and targets for further study of the upstream mechanism responsible for effector T cell imbalance.