This thesis investigates mice with genetic knock-outs in certain chemokines or their receptors which have shown signs of Age Related Macula Degeneration (AMD) by causing dysfunction to the immune response in the retina. We explored two mechanisms of retinal damage in mice lacking the chemokine, CCL2 or the chemokine receptor, CX3CR1. We tested the underlying retinal function and cellular and structural responses during aging and after light-induced oxidative damage to examine the role of these signaling pathways in the retina.