Project details

Age-related macular degeneration (AMD) is the leading cause of blindness in people aged 55 or over. In AMD, the cells of the retina become damaged due to increased accumulation of extracellular deposits, or drusen, and/or increased formation of blood vessels behind the retina. The cause of the disease is not known, but strong evidence suggests a role of inflammation as a trigger of retinal damage.

This study will investigate if and how auto-antibodies and immune complexes play a role in the disease. Immune complexes, formed when antibody bind to their antigen, are generally damaging to the host. Antibodies operate via specialised receptors called Fc receptors (FcγRs), expressed on macrophages and microglia and binding of immune complexes to these receptors can stimulate macrophages to release toxic inflammatory molecules that can contribute to tissue damage. Using a novel mouse model of the disease, that shows many characteristics of human AMD but with a much faster onset, the relative expression levels of different FcγRs in the healthy eye, and how these change during disease, will be investigated.
In another model the effect of FcγR deletion on the disease progression will be examined. These studies will be complemented by in vitro studies to investigate if antibodies from AMD patients show a similar effect on retinal damage.

This project will lead to better understanding of the immunological mechanisms in the eye, hopefully leading to novel or better treatments for AMD.