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引用本文:金仲田,张德恒,彭吉润,李澍,冷希圣. �����ص����������Է������Լ�״���׷��������е�����[J]. 中国实用外科杂志, 2003, 23(3): 143-145
作者姓名:金仲田  张德恒  彭吉润  李澍  冷希圣
作者单位:1. 北京大学人民医院肝胆外科中心,100044
2. 吉林大学中日联谊医院基本外科,长春,130032
摘    要:目的 探讨干扰素调节因子(IRF)-1在实验性自发免疫性甲状腺炎(EAT)发病及进展过程中的作用。方法 对6周龄NOD小鼠用佐剂混合的小鼠甲状腺球蛋白(mTg)免疫,4周后用相同剂量mTg加强免疫。再过4周取甲状腺和血清样本。甲状腺组织做HE染色,分析EAT的发病率及重症度。应用酶免疫测定(EIA)法测定血清T4值,评估甲状腺功能。采用酶联免疫吸附测定(ELISA)法测定血清抗小鼠甲状腺球蛋白抗体(anti-mTgAb)值,分析其结果,探讨与EAT重症度的关系。结果 Tg免疫组IRF-1+/+,+/-,-/-小鼠均比对照组显示EAT的高发倾向。在EAT重症度上,Tg免疫组比对照组明显增加,差异有显著的统计学意义,但与IRF-1基因型无相关性。Tg免疫组anti-mTgAb值比对照组上升,有统计学意义,但在IRF-1基因型之间未显示相关性。血清anti-mTgAb值与EAT重症度之间显示正相关关系。Tg免疫组血清T4值比对照组降低,有统计学意义,但在IRF-1基因型之间未显示相关性。结论 IRF-1-/-小鼠与IRF-1+/+,+/-小鼠均可诱发Tg免疫性EAT,说明在Tg免疫性EAT的发病过程中IRF-1的作用不大,证明IRF-1缺陷NOD小鼠在桥本病模型的病态分析中非常有价值。

关 键 词:发病机制 自发免疫性甲状腺炎 干扰素调节因子 甲状腺球蛋白 甲状腺球蛋白抗体
文章编号:1005-2205(2003)03-0143-03

The role of interferon regulatory factor in the etiology of autoimmune thyroiditis
Jin Zhongtian,Zhang Deheng,Peng Jirun,et al.. The role of interferon regulatory factor in the etiology of autoimmune thyroiditis[J]. Chinese Journal of Practical Surgery, 2003, 23(3): 143-145
Authors:Jin Zhongtian  Zhang Deheng  Peng Jirun  et al.
Affiliation:Jin Zhongtian*,Zhang Deheng,Peng Jirun,et al.*Department of Hepatobiliary Surgery,The People's Hospital,Peking University,Beijing 100044,China
Abstract:Objective To investigate the role of interferon regulatory factor(IRF)-1 in the development of experimental autoimmune thyroiditis(EAT). Methods Either thyroglobulin(Tg) or saline emulsified in an adjuvand was administered to mice at 6 and 10 weeks after birth. Thyroid tissue and sera were obtained from 14-week-old mice. HE staining has been emplyed to evaluate the incidence and severity of EAT.Serum anti-mouse thyroglobulin antibodies(anti-mTgAb) titers of mice was determined by ELISA and the relationship between EAT severity and anti-mTgAb titer was analyzed. The value of T4 in serum was determined by EIA for evaluation of the thyroid function.Results Tg-treated IRF-1+/+,+/-and-/-mice revealed higher incidence of the EAT than that of the control group.EAT severity of Tg-treated mice was significantly higher than that of the controlled, but was independent of the genotype of IRF-1. Anti-mTgAb titer of Tg-treated mice was significantly higher than that of the controlled, but was independent of the genotype of IRF-1. Serum anti-mTgAb titers was in proportion to the severity of the EAT. Serum T4 value of Tg-treated mice was significantly lower than that of the controlled,but was independent of the genotype of IRF-1.Conclusion Tg-immunised EAT could be induced in IRF-1-/-and+/+,+/-mice. These results suggest that IRF-1 plays a minor role in the pathogenesis of immunological EAT and IRF-1 lacking NOD mouse plays an important role in the analyses of the model of the Hashimoto's morbidity.
Keywords:Autoimmune thyroiditis Interferon regulatory factor Thyroglobulin Thyroglobulin antibodies
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