Autoimmune thyroid diseases (AITD) are group organ-specific autoimmune diseases with unknown etiology. Th1/Th2 cellular immune responses play an important role for the pathogenesis of AITD. To clarify the relationship between serum Th1/Th2 cytokines levels and autoantibodies against thyroid, and explore the role of Th1/Th2 cellular immunity imbalance in the pathogenesis of autoimmune thyroid diseases (AITD), we examined the serum level of Th1/ Th2 cytokines and autoantibodies in 21 patients with Graves' disease (GD), 18 cases with Hashimoto's thyroiditis (HT), 17 cases with non-toxic nodular goiter (NTNG) and 20 healthy subjects in this study. The serum concentrations of their Th1 cytokines (IFN-g, IL-2) and Th2 cytokines (IL-4, IL-10) were assayed by ELISA. The serum levels of their thyrotropin receptor antibodies (TRAb), thyroglobulin antibodies (TGAb) and thyroid peroxidase antibodies (TPOAb) were measured by routine methods. The relationship between the serum Th1 and Th2 cytokines levels and serum TRAb, TGAb and TPOAb levels were analyzed. Our results showed that the serum levels of IL-4 and IL-10 in patients with GD were significantly higher than those in patients with HT, NTNG and healthy subjects (P<0.01), while the serum levels of IFN-g and IL-2 in patients with HT were significantly higher than those in patients with GD, NTNG and healthy subjects (P<0.01), and serum IL-4 level was significantly lower than that in healthy subject as well (P<0.05). In GD patients, the serum levels of both IL-4 and IL-10 were positively associated with serum TRAb titer, respectively (r ¼ 0.683, 0.579; P < 0.05). In HT patients, the serum levels of both IFN-gand IL-2 were positively associated with serum TGAb and TPOAb titers, respectively (IFN-g: r ¼ 0.542, 0.650; IL-2: r ¼ 0.517, 0.602; P<0.05). These results suggest that the patients with GD or HT had a cellular immunity imbalance, with a Th2 cell immune response dominant in GD patients and a Th1 cell immune response dominant in HT patients.Recently, we reported that LTC4 synthesis enzymes including leukotriene C4 synthase (LTC 4 S), microsomal glutathione S-transferase (mGST) 2 and mGST3, could all conjugate LTA4 and reduced glutathione (GSH) to form LTC4, and were related to hepatic ischemia-reperfusion (I/R) injury. However, the gene expression mechanism of LTC4 synthesis enzymes during early hepatic I/R is largely unclear. Adult male Sprague-Dawley rats were divided into 2 groups: sham group (Sham), and ischemic-reperfusion group (I/R).
S51Abstracts / Cell Biology International 32 (2008) S1eS67
