视网膜新生血管性疾病是全球重要的致盲性眼病。众多研究表明，细胞因子及巨噬细胞参与调控新生血管的形成，其中M2型巨噬细胞促进新生血管性疾病的发展，而白细胞介素19(IL-19)可诱导体内外巨噬细胞向M2极化。我们前期研究发现，氧诱导视网膜病变（OIR）小鼠模型中的M2型巨噬细胞可促进视网膜病理性新生血管的形成，玻璃体腔注射抗IL-19抗体可显著抑制其发展。为进一步阐明IL-19在视网膜新生血管形成中的作用及机制，我们将利用OIR小鼠模型和人视网膜微血管内皮细胞，通过细胞和分子免疫学实验技术，探究IL-19对视网膜微血管内皮细胞功能的直接调控作用，及通过调控巨噬细胞M2极化对视网膜新生血管的间接作用，揭示IL-19对视网膜病理性新生血管和生理性血管重构的调控机制，探讨IL-19及其下游信号分子和细胞因子与M2极化和新生血管形成的关联性，为视网膜新生血管性疾病的治疗提供新靶点。

Retinal neovascular disease is a leading cause of blindness worldwide. Many studies showed that cytokines and macrophages participate in regulating neovascularization, M2 macrophages significantly promote progress of neovascular diseases, and interleukin-19 (IL-19) has been reported to promote M2 polarization of macrophages in vivo and in vitro. Our previous studies demonstrated that M2 macrophages enhanced retinal pathological neovascularization in a mouse model of oxygen-induced retinopathy (OIR). Moreover, intravitreal injection of anti-IL-19 antibody remarkably reduced the pathological neovascularization. To further clarify the effects and mechanisms of IL-19 in retinal neovascularization, we plan to use the OIR mouse model and human retinal microvascular endothelial cells, through experimental techniques of cellular and molecular immunology, to investigate the direct effects of IL-19 to retinal microvascular endothelial cells, as well as the indirect effects by regulating M2 polarization of macrophages in retinal neovascularization. We also plan to reveal the immunological mechanisms of IL-19 to retinal pathological neovascularization and physiological revascularization, and to explore the relevance among IL-19, its downstream signal molecules and cytokines, as well as M2 polarization of macrophages and neovascularization, which might provide new molecular targets for treating retinal neovascular disease.