Endo T, Haraguchi K, Ohmori M, Ikeda M, Ohta K, Onaya T
Third Department of Internal Medicine, University of Yamanashi Medical School, Japan.
Biochem Biophys Res Commun. 1991 Sep 30;179(3):1543-7. doi: 10.1016/0006-291x(91)91748-2.
There exists a consensus that hyperthyroid Graves' disease is caused by thyrotropin receptor (TSH-R) autoantibodies. To test the possibility that the TSH-R is the sole antigen for thyroid stimulating antibodies (TSAb), we compared bioactivities of Graves' IgGs between non-thyroid mammalian cells transfected with human TSH-R cDNA and the reference thyroid bioassay. A Graves' IgG with TSH-binding inhibitor immunoglobulin (TBII) activity (89%) markedly stimulated cAMP formation in both CHO-K1 cells transfected with TSH-R cDNA (340 microU/ml of TSH equivalent) and rat thyroid cells, FRTL-5, (410 microU/ml of TSH equivalent). In contrast, a TBII negative (-1.5%) IgG from another patient with Graves' disease showed a strong thyroid stimulating activity (87 microU/ml of TSH equivalent) when FRTL-5 cells were used for the assay. But no stimulating activity was observed in this IgG when CHO-K1 cells transfected with TSH-R cDNA were used, suggesting a possible existence of TSH-R non-mediated thyroid stimulating immunoglobulin in some cases of Graves' disease.
目前存在一种共识，即甲状腺功能亢进的格雷夫斯病是由促甲状腺素受体（TSH-R）自身抗体引起的。为了检验TSH-R是否是甲状腺刺激抗体（TSAb）的唯一抗原，我们比较了转染人TSH-R cDNA的非甲状腺哺乳动物细胞与参考甲状腺生物测定法中格雷夫斯病IgG的生物活性。一种具有促甲状腺素结合抑制免疫球蛋白（TBII）活性（89%）的格雷夫斯病IgG，在转染TSH-R cDNA的CHO-K1细胞（相当于340微单位/毫升促甲状腺素）和大鼠甲状腺细胞FRTL-5（相当于410微单位/毫升促甲状腺素）中均显著刺激了环磷酸腺苷（cAMP）的形成。相比之下，另一位格雷夫斯病患者的TBII阴性（-1.5%）IgG，在用FRTL-5细胞进行测定时显示出强烈的甲状腺刺激活性（相当于87微单位/毫升促甲状腺素）。但当使用转染TSH-R cDNA的CHO-K1细胞时，该IgG未观察到刺激活性，这表明在某些格雷夫斯病病例中可能存在TSH-R非介导的甲状腺刺激免疫球蛋白。
