Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis

Abstract Characterised by intraocular inflammation, non‐infectious uveitis includes a large group of autoimmune and autoinflammatory diseases that either involve the eye alone or have both ocular and systemic manifestations. When non‐infectious uveitis involves the posterior segment of the eye, spec...

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Main Authors: Lisia Barros Ferreira, Keryn A Williams, Giles Best, Cameron D Haydinger, Justine R Smith
Format: Article
Language:English
Published: Wiley 2023-01-01
Series:Clinical & Translational Immunology
Subjects:
Online Access:https://doi.org/10.1002/cti2.1479
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author Lisia Barros Ferreira
Keryn A Williams
Giles Best
Cameron D Haydinger
Justine R Smith
author_facet Lisia Barros Ferreira
Keryn A Williams
Giles Best
Cameron D Haydinger
Justine R Smith
author_sort Lisia Barros Ferreira
collection DOAJ
description Abstract Characterised by intraocular inflammation, non‐infectious uveitis includes a large group of autoimmune and autoinflammatory diseases that either involve the eye alone or have both ocular and systemic manifestations. When non‐infectious uveitis involves the posterior segment of the eye, specifically the retina, there is substantial risk of vision loss, often linked to breakdown of the inner blood‐retinal barrier. This barrier is formed by non‐fenestrated retinal vascular endothelial cells, reinforced by supporting cells that include pericytes, Müller cells and astrocytes. Across the published literature, a group of inflammatory cytokines stand out as prominent mediators of intraocular inflammation, with effects on the retinal endothelium that may contribute to breakdown of the inner blood‐retinal barrier, namely tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6, IL‐8, IL‐17 and chemokine C‐C motif ligand (CCL)2. This article reviews the function of each cytokine and discusses the evidence for their involvement in retinal endothelial barrier dysfunction in non‐infectious uveitis, including basic laboratory investigations, studies of ocular fluids collected from patients with non‐infectious uveitis, and results of clinical treatment trials. The review also outlines gaps in knowledge in this area. Understanding the disease processes at a molecular level can suggest treatment alternatives that are directed against appropriate biological targets to protect the posterior segment of eye and preserve vision in non‐infectious uveitis.
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spelling doaj.art-30d3384039c84a79a8bc7c05d367f71a2023-12-25T11:04:35ZengWileyClinical & Translational Immunology2050-00682023-01-011212n/an/a10.1002/cti2.1479Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitisLisia Barros Ferreira0Keryn A Williams1Giles Best2Cameron D Haydinger3Justine R Smith4Flinders University College of Medicine and Public Health Adelaide SA AustraliaFlinders University College of Medicine and Public Health Adelaide SA AustraliaFlinders University College of Medicine and Public Health Adelaide SA AustraliaFlinders University College of Medicine and Public Health Adelaide SA AustraliaFlinders University College of Medicine and Public Health Adelaide SA AustraliaAbstract Characterised by intraocular inflammation, non‐infectious uveitis includes a large group of autoimmune and autoinflammatory diseases that either involve the eye alone or have both ocular and systemic manifestations. When non‐infectious uveitis involves the posterior segment of the eye, specifically the retina, there is substantial risk of vision loss, often linked to breakdown of the inner blood‐retinal barrier. This barrier is formed by non‐fenestrated retinal vascular endothelial cells, reinforced by supporting cells that include pericytes, Müller cells and astrocytes. Across the published literature, a group of inflammatory cytokines stand out as prominent mediators of intraocular inflammation, with effects on the retinal endothelium that may contribute to breakdown of the inner blood‐retinal barrier, namely tumour necrosis factor (TNF)‐α, interleukin (IL)‐1β, IL‐6, IL‐8, IL‐17 and chemokine C‐C motif ligand (CCL)2. This article reviews the function of each cytokine and discusses the evidence for their involvement in retinal endothelial barrier dysfunction in non‐infectious uveitis, including basic laboratory investigations, studies of ocular fluids collected from patients with non‐infectious uveitis, and results of clinical treatment trials. The review also outlines gaps in knowledge in this area. Understanding the disease processes at a molecular level can suggest treatment alternatives that are directed against appropriate biological targets to protect the posterior segment of eye and preserve vision in non‐infectious uveitis.https://doi.org/10.1002/cti2.1479cytokineendothelial cellendotheliuminflammationretinauveitis
spellingShingle Lisia Barros Ferreira
Keryn A Williams
Giles Best
Cameron D Haydinger
Justine R Smith
Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis
Clinical & Translational Immunology
cytokine
endothelial cell
endothelium
inflammation
retina
uveitis
title Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis
title_full Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis
title_fullStr Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis
title_full_unstemmed Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis
title_short Inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non‐infectious uveitis
title_sort inflammatory cytokines as mediators of retinal endothelial barrier dysfunction in non infectious uveitis
topic cytokine
endothelial cell
endothelium
inflammation
retina
uveitis
url https://doi.org/10.1002/cti2.1479
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AT gilesbest inflammatorycytokinesasmediatorsofretinalendothelialbarrierdysfunctioninnoninfectiousuveitis
AT camerondhaydinger inflammatorycytokinesasmediatorsofretinalendothelialbarrierdysfunctioninnoninfectiousuveitis
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