De Groot L J, Shin Y Ha, Pan D, Gopalakrishnan G, Hennessey J V
Division of Endocrinology, Department of Medicine, Brown University, Providence, USA.
J Endocrinol Invest. 2009 Jan;32(1):52-6. doi: 10.1007/BF03345679.
In Graves' disease (GD) immunized T cells reactive to TSH-receptor epitopes contribute to pathogenesis through B cell help, and cytotoxicity. We evaluated T cell responses to synthetic TSH-receptor epitopes in hyperthyroid patients with GD prior to therapy, at 6-8 weeks after radioactive iodine (RAI) administration, or 6-8 months later when euthyroid, and in control subjects. All T cell responses were relatively low as generally found in human autoimmune diseases. Responses in hyperthyroid GD patients were significantly greater than among controls, were augmented 6-8 weeks after RAI treatment, were still present after patients became euthyroid, and did not differ between DR3+ and non-DR3+ patients. Patient's T cells reacted to multiple different epitopes, and reactivity differed depending on the course of the disease and treatment.While certain epitopes most commonly cause T cell reactivity, we did not find evidence for a single or few "dominant" epitopes.
在格雷夫斯病(GD)中,对促甲状腺激素受体表位产生反应的免疫T细胞通过辅助B细胞和细胞毒性作用参与发病机制。我们评估了未经治疗的甲状腺功能亢进的GD患者、放射性碘(RAI)给药后6 - 8周或甲状腺功能正常6 - 8个月后的GD患者以及对照受试者对合成促甲状腺激素受体表位的T细胞反应。所有T细胞反应相对较低,这在人类自身免疫性疾病中较为常见。甲状腺功能亢进的GD患者的反应显著高于对照组,RAI治疗后6 - 8周反应增强,患者甲状腺功能恢复正常后反应仍然存在,并且DR3 +和非DR3 +患者之间没有差异。患者的T细胞对多种不同表位产生反应,反应性因疾病进程和治疗而异。虽然某些表位最常引起T细胞反应性,但我们没有发现单一或少数“主导”表位的证据。