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Publication: C3 in the retina

Age-related macular degeneration (AMD) is the leading cause of blindness, costing the global economy 350 billion dollars annually. Dysfunction of the innate immune system, specifically the complement cascade, increases the risk of developing AMD by 70%. Due to this strong link between complement and AMD, it is important to investigate the cellular sources of complement proteins within the retina, in order to develop better therapeutics for this disease. In this study, we demonstrate the role of macrophages in the emergence of a retinal lesion. We show that these immune cells deposit complement proteins in the damaged photoreceptor layer, which contributes to further degeneration. Using novel approaches to inhibit complement gene expression in the retina, we demonstrate that inhibition of macrophage activity may slow the rate of retinal lesion development, as seen in the more prevalent form of AMD. Our data highlight the potential of gene therapies to manage complement activation in retinal degenerations including AMD.

For the complete article published in IOVS (June, 2017), please follow this link:

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