Analysis of thyroid function in rats specifically expressing MHC class II and B7.1 in the thyroid

为了探讨MHC-II类抗原和共刺激分子B7.1在Graves病发病机制中的作用，我们制备了甲状腺球蛋白启动子衍生的II类反式激活基因(CIITA)和B7.1基因。我们培育出了这些基因的转基因大鼠。转CIITA基因大鼠血清T_3水平与对照大鼠无明显差异，且未检测到甲状腺刺激性抗体(TSAb)活性。我们进一步获得了在甲状腺中特异性表达MHC II类和B7.1的转基因大鼠。然而，在这些大鼠中也没有观察到TSAb活性。这些结果表明，促甲状腺激素受体和MHC-II类抗原在甲状腺中的共表达不足以产生TSAb。

In order to investigate the role of MHC class II antigen and co-stimulatory molecule, B7.1, in the pathogenesis of Graves' disease, we prepared thyroglobulin promoter derived class II transactivator gene (CIITA) and also B7.1 gene. We produced transgenic rats of these gene. No difference was observed in the serum T3 between CIITA transgenic and the control rats, and we could not observed thyroid stimulating antibody (TSAb) activity in the sera of these transgenic animals. We further obtained transgenic rats specifically expressing both MHC class II and B7.1 in the thyroid. However, no TSAb activity was also observed in these rats. These results indicate that co expression of thyrotropin receptor and MHC class II antigen in thyroid gland is not sufficient to produce TSAb.