Vitti P, Chiovato L, Tonacchera M, Bendinelli G, Mammoli C, Capaccioli A, Giachetti M, Pinchera A
Istituto di Endocrinologia, Università di Pisa, Italia.
Thyroidology. 1992 Apr;4(1):49-51.
Some authors have suggested a role of autoimmunity in the pathogenesis of iodine deficiency disorders (IDD). For this purpose we have searched for thyroid adenylate cyclase stimulating antibody (TSAb) and thyroid growth stimulating antibody (TGSAb) in patients with endemic goiter (EG) and endemic cretinism (EC). Immunoglobulins G preparations (IgGs) were tested in FRTL-5 cells. TSAb were calculated as percent of cAMP increase over basal production and TGSAb were expressed as percent of increase of 3H-thymidine incorporation and DNA content in FRTL-5 cells. Our results show that IgGs from goitrous patients were devoid of TSAb and TGSAb activities, while in the same conditions IgGs from patients with Graves' disease had the ability to stimulate cAMP production and 3H-thymidine incorporation in FRTL-5 cells. These data argue against a direct role of TSAb and TGSAb in the pathogenesis of IDD.
一些作者认为自身免疫在碘缺乏症（IDD）的发病机制中起作用。为此，我们在地方性甲状腺肿（EG）和地方性克汀病（EC）患者中寻找甲状腺腺苷酸环化酶刺激抗体（TSAb）和甲状腺生长刺激抗体（TGSAb）。在FRTL-5细胞中检测免疫球蛋白G制剂（IgGs）。TSAb以cAMP增加量占基础产量的百分比计算，TGSAb以FRTL-5细胞中3H-胸腺嘧啶核苷掺入量和DNA含量增加的百分比表示。我们的结果表明，甲状腺肿患者的IgGs缺乏TSAb和TGSAb活性，而在相同条件下，格雷夫斯病患者的IgGs有能力刺激FRTL-5细胞中cAMP的产生和3H-胸腺嘧啶核苷的掺入。这些数据表明TSAb和TGSAb在IDD发病机制中没有直接作用。
