Contribution of Interleukin-17A to Retinal Degenerative Diseases

Abstract

Retinal degenerative diseases are a leading cause of vision loss and blindness throughout the world, characterized by chronic and progressive loss of neurons and/or myelin. One of the common features of retinal degenerative diseases and central neurodegenerative diseases is chronic neuroinflammation. Interleukin-17A (IL-17A) is the cytokine most closely related to disease in its family. Accumulating evidence suggests that IL-17A plays a key role in human retinal degenerative diseases, including age-related macular degeneration, diabetic retinopathy and glaucoma. This review aims to provide an overview of the role of IL-17A participating in the pathogenesis of retinal degenerative diseases, which may open new avenues for potential therapeutic interventions.

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“…IL-17A promotes retinal inflammation and damage by inducing the production of proinflammatory cytokines, such as IL-1β, IL-6, and TNF-α ( Byrne et al, 2021 ), and by increasing oxidative stress and vascular permeability in the retina ( Sigurdardottir et al, 2019 ). IL-17A also contributes to the breakdown of the blood–retinal barrier (BRB), which is a protective barrier that helps maintain the proper environment for the retina to function ( Zhong and Sun, 2022 ). In DR, the breakdown of the BRB can lead to the leakage of fluids and blood into the retina, which can contribute to retinal damage and vision loss ( Rudraraju et al, 2020 ).…”

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“…Interleukin‐17 receptors are heterodimeric structures composed of the IL‐17 receptor A (IL‐17RA) plus a second chain, IL17‐RC, which confers ligand and signalling specificity 143 . Interleukin‐17RA is widely expressed, while IL17‐RC is expressed by non‐immune cells, which in the retina include Müller cells, retinal endothelial cells and photoreceptors 144,145 . Interleukin‐17 binds to the IL‐17RA/IL17‐RC receptor complex, initiating an interaction between the cytoplasmic SEFIR domains of the receptor and the signalling adaptor protein Act1, which recruits TRAF6 and activates signalling via the NF‐κB, MAPK, ERK, JAK/PI3K, JAK/STAT, p38, JNK and CCAAT‐enhancer‐binding protein (C/EBPs) pathways 140,143 .…”

“… 143 Interleukin‐17RA is widely expressed, while IL17‐RC is expressed by non‐immune cells, which in the retina include Müller cells, retinal endothelial cells and photoreceptors. 144 , 145 Interleukin‐17 binds to the IL‐17RA/IL17‐RC receptor complex, initiating an interaction between the cytoplasmic SEFIR domains of the receptor and the signalling adaptor protein Act1, which recruits TRAF6 and activates signalling via the NF‐κB, MAPK, ERK, JAK/PI3K, JAK/STAT, p38, JNK and CCAAT‐enhancer‐binding protein (C/EBPs) pathways. 140 , 143 Increased activity of these pathways leads to the transcription of inflammatory cytokines, chemokines and antimicrobial peptides.…”

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“…Angiogenesis is linked to the development of numerous illnesses and plays an important part in normal physiological activities such as embryo development, wound healing, and the menstrual cycle [99]. The dysregulation of angiogenesis is widely established to cause the onset and progression of a variety of illnesses, including rheumatoid arthritis, psoriasis, diabetic retinopathy, malignant tumors, and age-related macular degeneration (AMD) [100]. Angiogenesis is essential for the beginning, growth, and spread of malignancies because tumor cells require oxygen, nutrition, and growth factors for proliferation and development [101].…”