2-STEP DEVELOPMENT OF HASHIMOTO-LIKE THYROIDITIS IN GENETICALLY AUTOIMMUNE-PRONE NONOBESE DIABETIC MICE - EFFECTS OF IODINE-INDUCED CELL NECROSIS
2-STEP DEVELOPMENT OF HASHIMOTO-LIKE THYROIDITIS IN GENETICALLY AUTOIMMUNE-PRONE NONOBESE DIABETIC MICE - EFFECTS OF IODINE-INDUCED CELL NECROSIS
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DOI：
10.1677/joe.0.1470311
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发表时间：
1995-11-01
影响因子：
4
通讯作者：
DENEF, JF
中科院分区：
文献类型：
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作者：
MANY, MC;MANIRATUNGA, S;DENEF, JF
已知对甲状腺肿小鼠施用高剂量碘化物（HID；10μg/天）会诱导甲状腺细胞坏死和炎症，而在大多数品系中，这种情况是短暂的。在这项研究中，我们分析了碘化物对自身免疫倾向的非肥胖糖尿病 (NOD) 小鼠的影响。喂食标准饮食（MID；1 μg I/天）或 HID 的对照 NOD 小鼠不会自发患上甲状腺炎。在先前导致甲状腺肿大的 NOD 小鼠中，HID 在 4 天内引发甲状腺细胞坏死和弥漫性炎症。炎症细胞由 MHC II+ 类抗原呈递细胞、CD4+ T 辅助细胞和 CD8+ T 抑制/细胞毒性细胞组成。 HID治疗96天后，100%的动物出现类似于桥本氏病的甲状腺炎，甲状腺滤泡、大簇T和B细胞以及血浆中的抗甲状腺抗体被破坏。用MID治疗甲状腺肿小鼠时，没有观察到细胞坏死，也没有获得自身免疫性甲状腺炎。因此，早期碘诱导的细胞坏死和炎症可能被认为是携带自身免疫性疾病遗传易感性的个体中诱导和持续存在自身免疫性甲状腺炎的重要因素。
The administration of a high iodide dose (HID; 10 mu g/day) to goitrous mice is known to induce thyroid cell necrosis and inflammation, which, in most strains, is transient. In this study, we analyzed the effects of iodide in autoimmune prone non-obese diabetic (NOD) mice.Control NOD mice fed a standard diet (MID; 1 mu g I/day) or HID did not spontaneously develop thyroiditis. In NOD mice previously made goitrous, HID provoked thyroid cell necrosis and diffuse inflammation within 4 days. Inflammatory cells consisted of MHC-class II+ antigen-presenting cells, CD4+ T helper cells and CD8+ T suppressor/cytotoxic cells. After 96 days of treatment with HID, thyroiditis similar to Hashimoto's disease was obtained in 100% of the animals, with destruction of thyroid follicles, large clusters of T and B cells, and antithyroid antibodies in the plasma. When treating goitrous mice with MID, no cell necrosis was observed and no autoimmune thyroiditis was obtained. The early iodide-induced cell necrosis and inflammation may thus be considered as an important factor in the induction and persistence of autoimmune thyroiditis in individuals carrying a genetic susceptibility to autoimmune disease.