碘对诱发易感和非易感小鼠自身免疫性甲状腺炎的实验研究

The role of iodine in the induction of EAT in susceptible and unsusceptible mice

目的 研究碘对实验性自身免疫性甲状腺炎 ( EAT)易感和非易感小鼠诱发 EAT的影响 ,进一步探讨自身免疫性甲状腺疾病 ( AITD)发病的机理。方法 采用 EAT易感 ( TA- 1)和非易感 ( BAL B/ c)小鼠经甲状腺球蛋白 ( Tg)免疫 ,诱发为 EAT实验动物模型并给予不同水平的碘饮食。观察小鼠甲状腺组织的病理改变和炎细胞浸润程度、血清中 Tg自身抗体的水平以及低碘和高碘 Tg抗原性的不同。结果 12种品系小鼠经 Tg诱发 ,均出现不同水平的 Tg自身抗体和甲状腺的炎症反应 ,血清中 Tg自身抗体的出现早于甲状腺的病理改变。 2TA- 1小鼠的甲状腺炎症反应明显高于 BAL B/ c小鼠 ,高碘组中的 TA- 1小鼠炎症较适碘组更明显 ,为弥漫性伴慢性炎症 ( +++)。 3高碘 Tg诱发的 Tg抗体与高碘 Tg抗原的反应明显高于与低碘 Tg抗原的反应 ,低碘 Tg诱发的 Tg抗体反之 ,表明二者抗原性有所不同。结论 高碘摄入会使易感小鼠 EAT的发病加重 ,其机理除了体内的遗传因素 ,可能与过度碘化的 Tg抗原性增强有关。

Objective To study the relationship between the iodine and gene predisposition in the invasion of AITD and thus to further understand the pathogenesis of this disease.Methods EAT model was established by immunization with thyrogloblin in EAT susceptible (TA-1) and unsusceptible (BALB/c) mice and the role of iodine in this induction process was evaluated.Results ①Different levels of anti-Tg autoantibody in sera and the inflammation reaction in thyroid glands could equally be found in these two strains after induction, and the former seemed much earlier to be observed than the latter.②The inflammation reaction in thyroid glands was significantly higher in TA-1 mice than in BALB/c mice and the severest inflammation reaction was found in TA-1 mice from high iodine group. HI-Tg facilitated EAT model's establishing than LI-Tg.③Anti-Tg autoantibody produced by immunizing with HI-Tg reacted much higher with H I-Tg than with LI-Tg, while immunizing with LI-Tg got the reverse results, which indicated the different antigenicity between them.Conclusions High iodine intake aggravates the disease on susceptible animals, the mechanism of which, besides the gene predisposition, may be related with the higher antigigenicity of over-iodized Tg as well.