Treatment with interleukin‐33 is non‐toxic and protects retinal pigment epithelium in an ageing model of outer retinal degeneration |
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Authors: | Alison J Clare David A Copland Lindsay B Nicholson Jian Liu Chris R Neal Stephen Moss Andrew D Dick Sofia Theodoropoulou |
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Affiliation: | 1.
Academic Unit of Ophthalmology, Translational Health Sciences, University of Bristol, Bristol
UK
;
2.
School of Cellular and Molecular Medicine, University of Bristol, Bristol
UK
;
3.
Wolfson Bioimaging Facility, University of Bristol, Bristol
UK
;
4.
UCL Institute of Ophthalmology, London
UK
;
5.
NIHR Biomedical Research Centre of Ophthalmology, Moorfields Eye Hospital, London
UK
;
6.
Department of Ophthalmology, Cheltenham General Hospital, Cheltenham
UK |
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Abstract: | The leading cause of central vision loss, age‐related macular degeneration (AMD), is a degenerative disorder characterized by atrophy of retinal pigment epithelium (RPE) and photoreceptors. For 15% of cases, neovascularization occurs, leading to acute vision loss if left untreated. For the remaining patients, there are currently no treatment options and preventing progressive RPE atrophy remains the main therapeutic goal. Previously, we have shown treatment with interleukin‐33 can reduce choroidal neovascularization and attenuate tissue remodelling. Here, we investigate IL‐33 delivery in aged, high‐fat diet (HFD) fed mice on a wildtype and complement factor H heterozygous knockout background. We characterize the non‐toxic effect following intravitreal injection of IL‐33 and further demonstrate protective effects against RPE cell death with evidence of maintaining metabolic retinal homeostasis of Cfh+/−~HFD mice. Our results further support the potential utility of IL‐33 to prevent AMD progression. |
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Keywords: | age‐ related macular degeneration complement factor H IL‐ 33 retinal pigment epithelium |
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