甲状腺相关眼病（TAO）是目前发病率最高的成人眼眶疾病，病理表现为眶内脂肪体积增加和眼外肌纤维化，严重影响患者容貌外观和身心健康。目前TAO的发病机制并不清楚，目前公认的自身抗体是TSHR和IGF-1R，靶细胞为眼眶成纤维细胞。我们在既往的国家自然科学基金项目的研究中发现，炎性相关因子PTX-3在TAO患者的眼眶脂肪组织中高表达，TSH可以上调纤维细胞表达PTX-3，抗炎药物地塞米松可以阻断该诱导作用，IGF-1R信号通路抑制剂IH7和RV-001也可以阻断该诱导作用。本课题拟进一步研究PTX-3在TAO中的作用及其发挥作用的分子机制，为TAO的防治提供新的方向。

Thyroid associated ophthalmopathy（TAO）is one kind of orbital disease with the highest morbidity in adult. The main pathological changes are the expansion of the orbital adipose tissue and fibrosis of the extraocular muscles, which cause discomfort feelings and decreasing visual acuity. The mechanism of the disease is still beyond the scope. TSHR and IGF-1R are thought to be the main autoimmunity antibodies while orbital fibroblasts the main target cells. What we learned from the previous projects granted by NSFC is that inflammation related factor PTX-3 was higher expressed in orbital adipose tissue from TAO patients. Fibrocytes expressed higher level of PTX-3 after stimulated by TSH. Inhibitors of IGF-1R signaling pathway- 1H7 and RV-001 blocked the up-regulation of PTX-3 mRNA so as what anti-inflammation medicine dexamethasone did. This project intends to explore the role and mechanism of PTX-3 in TAO, which maybe helpful for the prevention and therapy of TAO.