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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 mT gAb)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。
Objective To investigate the role of interferon regulatory factor (IRF) 1 in the pathogenesis and progression of experimental autoimmune thyroiditis (EAT). Methods Six-week-old NOD mice were immunized with adjuvant-administered mouse thyroglobulin (mTg) and boosted with the same dose of mTg four weeks later. Thyroid and serum samples were taken in another 4 weeks. Thyroid tissue to do HE staining, analysis of the incidence and severity of EAT. Serum T4 value was measured by enzyme immunoassay (EIA) method to evaluate thyroid function. Serum anti-mouse anti-mT gAb was measured by enzyme-linked immunosorbent assay (ELISA), and the results were analyzed. The relationship between serum anti-mouse thyroid globulin antibody and severity of EAT was analyzed. Results Compared with the control group, IRF 1 + / +, + / -, - / - mice in Tg immunized group showed the tendency of EAT. In EAT severity, the Tg immunization group increased significantly compared with the control group, the difference was statistically significant, but no correlation with the IRF1 genotype. The anti-TgTbAb values in the Tg immunized group were significantly higher than those in the control group, but no correlation was found between the IRF1 genotypes. Serum anti-mTgAb values showed a positive correlation with severity of EAT. The serum T4 value of Tg immunized group was lower than that of control group, but there was no correlation between IRF1 genotypes. Conclusion IRT 1 / / +, + / - mice can induce Tg immune EAT, indicating that the role of IRF 1 in the pathogenesis of Tg immune EAT is not significant, and IRF 1 deficient NOD Mice are very valuable in the pathological analysis of the Hashimoto’s disease model.