Is IL-10 a Good Target to Inhibit Choroidal Neovascularisation in Age-Related Macular Disease?

A ge-related macular disease (AMD) occurs most frequently in people aged 60 years and older and affects the central part of the retina, causing distortion or loss of central vision. The disease is the leading cause of blindness in people aged 60 years and older in the developed world and causes milder visual loss in a much greater number (about 25 percent of people aged 60 years and older in the developed world have some degree of visual loss because of AMD). AMD generally involves both eyes, although they may not be affected at the same time or to the same degree. There are two forms of AMD: dry and wet. About 90 percent of patients with AMD have the dry atrophic type, for which there is currently no treatment, while 10 percent have wet AMD. Wet AMD causes the most severe visual loss and is the most aggressive form of the disease. In the wet form, choroidal blood vessels grow into the retina (choroidal neovascularisation [CNV]) but do not have the characteristic tight barriers of normal retinal blood vessels and so leak fl uid into the retina. Such leakage often occurs under the central part of the retina—the macula—which is needed for visual detail. Scar tissue follows and leads to permanent severe visual loss. In recent years, new forms of treatment for wet AMD have come into clinical practice following clinical trials. These new treatments are: (1) vitamins (the Age Related Eye Disease Study found that taking high levels of antioxidants and zinc can reduce the risk of developing advanced AMD by about 25 percent [1]); photodynamic therapy; and the most recently developed treatment, anti–vascular endothelial growth factor (anti-VEGF), which, when injected into the vitreous, has been helpful in preventing further visual loss and new vessel regression [2]. In a study published in PLoS Medicine , Apte et al. examined the role of the macrophage component of the infl ammatory response in CNV [3]. They used a mouse model in which CNV was induced in the eye with laser burns. In this mouse model, they looked at the possible role in CNV formation of the anti-infl ammatory cytokine IL-10, which inhibits T cell and macrophage functions. The researchers found that mice that were defi cient in IL-10 (IL-10 −/− mice) had increased infl ammation and decreased amounts of CNV compared with wild-type mice. Systemic neutralisation of IL-10 in the …