摘要
目的研究瘦素在实验性自身免疫性甲状腺炎(EAT)发病中的免疫调节机制。方法采用C57BL/6J小鼠在外源性瘦素干预下诱发EAT,观察小鼠甲状腺组织病理改变、血清中甲状腺过氧化物酶抗体(TPO-Ab)、甲状腺球蛋白抗体(Tg-Ab)和瘦素水平以及脾脏中IFN-γ和IL-4mRNA表达水平。结果小鼠经外源性瘦素干预后,其血清中瘦素水平高于EAT组和对照组,实验性自身免疫性甲状腺炎的发病率和甲状腺组织中炎细胞浸润程度也较直接诱发EAT组明显增高。瘦素干预诱发EAT组小鼠脾脏中IFN-γmRNA表达水平较EAT组明显升高(P=0.029),而IL-4mRNA表达水平在两组间比较无明显变化。两实验组小鼠血清中TPO-Ab和Tg-Ab水平均明显高于未诱发EAT对照组,但两组间比较均未见明显差异。结论瘦素对于Th1/Th2免疫平衡的影响在实验性自身免疫性甲状腺炎的发生、发展中有重要的免疫调节作用。
[Objective] To study the influence of leptin on the induction of experimental autoimmune thyroiditis （EAT）. [ Methods ] Female C57BL/6J mice were injected intraperitoneally with rmleptin or PBS starting 3 days before the induction of EAT. Histological severity of thyroid specimens was evaluated. The serum levels of TPO-Ab, Tg-Ab and leptin were measured. The expression level of IFN-γ/IL-4 mRNA in spleen were assayed. [ Results ] The serum level of leptin was higher in leptin-treated group than other two groups. The leptin-treated group developed more severe thyroiditis compared with PBS-treated group. There were no differences in IL-4 mRNA expression between leptin- and PBS-treated groups, while leptin did increase IFN-γ mRNA expression in leptin-treated group. Meanwhile, high serum levels of TPO-Ab and Tg-Ab were presented in the experimental groups. [ Conclusion ] Leptin contributes to the induction of EAT by tilting the balance between Thl and Th2 responses toward Thl responses.
出处
《中国现代医学杂志》
CAS
CSCD
北大核心
2009年第18期2733-2736,共4页
China Journal of Modern Medicine
