以脉络膜新生血管(CNV)为特征的湿性年龄相关黄斑变性（AMD）是难治性致盲眼病，确切机制尚不清楚。申请者新近发现在实验性CNV中，脉络膜组织中Tie2+巨噬细胞以及与其相关的Ang-2和CSF-1因子明显增加，提示其可能参与CNV的病理过程。鉴此，本研究旨在：①以激光诱导CNV模型，利用Tie2及Tie2+巨噬细胞敲除小鼠，检测Tie2+巨噬细胞在CNV中的作用和机制；②以Tie2+巨噬细胞培养上清液体外刺激人视网膜及脉络膜毛细血管内皮细胞，检测其血管网形成、细胞迁移、增殖和凋亡等的变化；③检测AMD患者外周血Tie2+巨噬细胞及相关因子的变化及其与治疗预后的相关性。综合分析明确Tie2+巨噬细胞在AMD发病过程中的确切作用和机制，为建立基于Tie2+巨噬细胞的AMD免疫干预新思路奠定基础。

Age related macular degeneration (AMD) is one of the leading causes of severe vision loss characterized by the choroidal neovascularization (CNV). Published data suggest that Tie2+ macrophages are involved in pathological process of various kinds of angiogenesis, while little is currently known about the roles of Tie2+ macrophages in the pathological process of CNV. We recently found during laser induced CNV, the number of Tie2+ macrophages and its associated factors (Ang-2 and CSF-1) in chaoridal were significantly enhanced than control mice. Therefore, we hypothesized that Tie2+ macrophages play critical roles in the pathological process of CNV. The aims of this study are: firstly, by laser-induced choroidal neovascularization model and using Tie2+ macrophage knock out mice and Tie2 knock out mice to inhibit Tie2+ macrophage infiltration, and to determine the roles of Tie2+ macrophage in laser induced CNV. Secondly, evaluate the human retinal endothelial cell (HREC) or human choroidal endothelial cell (HCEC) tube formation, migration, proliferation and apoptosis under the stimuli of culture supernatant from Tie2+ macrophages. Finally, examine the number of Tie2+ macrophages in peripheral blood from AMD patients and analyze the correlation between Tie2+ macrophages and AMD prognosis. Our study may provide clinical theoretical reference for choroidal neovascular diseases based on the Tie2+ macrophages intervention.