Abstract
AbstractGrowing evidences indicates that inflammation play an important role in AMD. In particular, subretinal mononuclear phagocytes (MPs) accumulate in the vicinity of the atrophic lesion of GA patients and are thought to contribute to photoreceptor degeneration. The mechanism by which MP participates to neuronal cell loss is currently unknown and no treatment is available to date to delay degeneration. We have recently shown that subretinal MPs that originate from the blood circulation and accumulate in the subretinal space are particularly detrimental in animal models of subretinal inflammation. Defects in the CX3CR1/CX3CL1 axis have been associated in animals with cardinal features of AMD including photoreceptor loss. We here show that CX3CR1 deficiency resulted in an exacerbated neurotoxicity of subretinal MPs. we present evidences that CX3CR1‐/‐ deficiency lead to the differentiation of subretinal MPs into an exacerbated pro‐inflammatory profile. Inhibiting neurotoxic mediators produced by subretinaly differentiated monocytes efficiently reduces photoreceptor loss in vitro and in animal models where MP accumulates. Our result provides new rationales to protect retina from damaging age‐dependent subretinal inflammation.
Published Version
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