中文摘要：

目的应用主要组织相容性复合物（MHC）Ⅱ与人TSH受体（TSHR）共表达细胞（hM12细胞）模拟Graves病（GD）时的甲状腺细胞，免疫C57BL／6小鼠，诱导GD动物模型，以研究异常表达于GD患者甲状腺滤泡上皮细胞上的MHC—Ⅱ分子是否是GD的致病因素。方法试验组C57BL／6小鼠8只，用hM12细胞进行腹腔免疫，每2周1次，共6次，对照组C57BL／6小鼠5只，用M12细胞免疫，方法同试验组。受试小鼠末次免疫5周后，检测以下指标：甲状腺激素水平；甲状腺刺激性抗体（TSAb）；甲状腺组织学检查。结果C57BL／6小鼠试验组2／8小鼠诱导为Graves甲亢。C57BL／6小鼠的T细胞（MHC—Ⅱ为H-2^b）不能识别由hM12细胞（H～2^d）提呈的抗原，C57BL／6小鼠出现GD样变化可能是hM12细胞表达的TSHR被小鼠体内职业性抗原递呈细胞（APCs）获取，经加工处理提呈给T细胞，诱发自身免疫反应的结果。结论异常表达于GD患者甲状腺滤泡上皮细胞上的MHC—Ⅱ分子可能与GD的发病无关，而是一种自身免疫反应的继发现象。

英文摘要：

Objective C57BL/6 mice （H-2b） were immunized with hM12 cells, which co-expressing major histocompatibility complex（MHC） class Ⅱ molecules and human thyrotropin reeeptor（TSHR） molecules, to development animal model of Graves＇ disease （GD） and to conjecture whether MHC class Ⅱ molecules expression by the human epithelial thyroid cell in GD would contribute to the pathogenesis of GD. Methods C57BL/6 mice in experimental groups（H-2^b） were immunized i.p. per 2 weeks with hM12 cells for six times, while mice in control groups were immunized with M12 cell. Five weeks later, the thyroids were histologically examined, and serum samples were tested for thyroid-stimulating antibodies （TSAb） and thyroid hormone levels. Results Two C57BL/6 mice in experiment groups developed Graves＇ disease change. T cells of C57BL/6 mice could not recognize the hTSHR presented by hM12 cells because of different H-2 molecules, hTSHR expressed by hM12 cells may be treated by professional APCs of C57BL/6 mice, then presented to T cells and induced Graves＇ -like disease. Conclusion MHC class Ⅱ molecules expressed on human epithelial thyroid cell in GD might not be a pathogenic factor of GD, but a secondary phenomenon induced by other immune disturbance.