Correlation between serum 25-(OH)D level and immune imbalance of Th1/Th2 cytokines in patients with Hashimoto's thyroiditis and its effect on autophagy of human Hashimoto thyroid cells.

The study aimed to determine the relationship between serum 25-(OH)D and Th1/Th2 cytokine immune imbalance, and the effect of 25-(OH)D on the autophagy of human Hashimoto thyroid cells. Western blot analysis was used to detect the expression levels of microtubule-associated protein 1 light chain 3 (LC3) and autophagy-associated protein mammalian target protein of rapamycin (mTOR) in thyroid tissues of 20 Hashimoto's thyroiditis (HT) patients and normal tissues of 20 benign thyroid adenomas. Nthy-ori3-1 cells (normal cells of human thyroid follicular epithelium) were treated with different concentrations of 25-(OH)D for 24 h. The expression of LC3, mTOR and caspase-3 protein in the cells was detected by western blot analysis. The apoptosis and proliferation levels were detected by flow cytometry and MTT assay, respectively. The levels of FT3, FT4 and IL-10 in the HT group were lower than those in the healthy control group. The serum levels of 25-(OH)D, TPOAb and TGAb in the HT group were lower than those in the healthy control group. Serum 25-(OH)D level in the HT group was negatively correlated with IL-2 and IFN-γ, and positively correlated with IL-4. In Hashimoto's thyroiditis tissues, the expression of mTOR was higher while the expression of LC3B-II was lower than that of normal thyroid tissue. With the increase in 25-(OH)D concentration, the expression level of mTOR increased, the expression level of LC3B-II decreased and the apoptosis rate was significantly increased. The cell proliferation rate decreased with the increase in 25-(OH)D concentration. The serum 25-(OH)D level in HT hypothyroidism patients was significantly lower than that of the control group. Thus, 25-(OH)D may be involved in the disease progression by upregulating the levels of Th1 cytokines and downregulating the levels of Th2 cytokines. 25-(OH)D can inhibit autophagy of thyroid cells, induce apoptosis and participate in the pathogenesis of Hashimoto's thyroiditis.