Age-related macular degeneration (AMD) is the most common disease leading to acquired blindness in developed countries. Choroidal neovascularization (CNV) is a characteristic of AMD and is induced by regional inflammation as a result of age-related conformational changes of the chorioretinal interface. Genome-wide association studies have provided evidence that the immune system is involved in the pathogenesis of AMD; however, the role of inflammatory cytokines in CNV has not been well established. We have demonstrated IL-27, a member of the IL-6/IL-12 cytokine family, has an angiostatic effect and regulates the development of laser-induced experimental CNV in mice. We also demonstrated IL-17 had a strong potential for promoting neovascularization in a vascular endothelial growth factor-independent manner in laser-induced experimental CNV in mice. Infiltrated γδT cells and Thy-1(+) innate lymphoid cells were the main sources of IL-17 in injured eyes. In addition, subretinal fibrosis is another problem of AMD. It is an end stage of AMD, characterized by fibrous membrane formation after choroidal neovascularization. An initial step of the pathogenesis is an epithelial-mesenchymal transition (EMT) of retinal pigment epithelium cells. We have demonstrated several cytokines, including IL-6, have involved in this later phase of AMD. Collectively, cytokines plays an important role in the AMD pathogenesis, and it may be a new target to regulate regional cytokines in the eye.