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了解趋化因子和细胞因子在单纯疱疹性角膜炎实验模型中的作用。

Understanding the Role of Chemokines and Cytokines in Experimental Models of Herpes Simplex Keratitis.

机构信息

Department of Ophthalmology, Saint Louis University, Saint Louis, MO, USA.

出版信息

J Immunol Res. 2017;2017:7261980. doi: 10.1155/2017/7261980. Epub 2017 Apr 9.

DOI:10.1155/2017/7261980
PMID:28491875
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5401741/
Abstract

Herpes simplex keratitis is a disease of the cornea caused by HSV-1. It is a leading cause of corneal blindness in the world. Underlying molecular mechanism is still unknown, but experimental models have helped give a better understanding of the underlying molecular pathology. Cytokines and chemokines are small proteins released by cells that play an important proinflammatory or anti-inflammatory role in modulating the disease process. Cytokines such as IL-17, IL-6, IL-1, and IFN- and chemokines such as MIP-2, MCP-1, MIP-1, and MIP-1 have proinflammatory role in the destruction caused by HSV including neutrophil infiltration and corneal inflammation, and other chemokines and cytokines such as IL-10 and CCL3 can have a protective role. Most of the damage results from neutrophil infiltration and neovascularization. While many more studies are needed to better understand the role of these molecules in both experimental models and human corneas, current studies indicate that these molecules hold potential to be targets of future therapy.

摘要

单纯疱疹性角膜炎是由单纯疱疹病毒 1 引起的角膜疾病。它是世界上导致角膜盲的主要原因。其潜在的分子机制尚不清楚,但实验模型有助于更好地理解潜在的分子病理学。细胞因子和趋化因子是细胞释放的小蛋白,在调节疾病过程中发挥重要的促炎或抗炎作用。细胞因子如 IL-17、IL-6、IL-1 和 IFN,以及趋化因子如 MIP-2、MCP-1、MIP-1 和 MIP-1 在 HSV 引起的破坏中具有促炎作用,包括中性粒细胞浸润和角膜炎症,而其他趋化因子和细胞因子如 IL-10 和 CCL3 可以发挥保护作用。大多数损伤是由中性粒细胞浸润和新生血管形成引起的。虽然还需要更多的研究来更好地了解这些分子在实验模型和人角膜中的作用,但目前的研究表明,这些分子有可能成为未来治疗的靶点。

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本文引用的文献

1
Herpes simplex virus keratitis: an update of the pathogenesis and current treatment with oral and topical antiviral agents.单纯疱疹病毒性角膜炎:发病机制及口服和局部用抗病毒药物当前治疗方法的最新进展
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Controlling herpetic stromal keratitis by modulating lymphotoxin-alpha-mediated inflammatory pathways.通过调节淋巴毒素-α介导的炎症途径控制疱疹性基质性角膜炎。
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Role of miR-132 in angiogenesis after ocular infection with herpes simplex virus.miR-132 在单纯疱疹病毒眼部感染后血管生成中的作用。
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IL-17A differentially regulates corneal vascular endothelial growth factor (VEGF)-A and soluble VEGF receptor 1 expression and promotes corneal angiogenesis after herpes simplex virus infection.IL-17A 差异调节角膜血管内皮生长因子 (VEGF)-A 和可溶性 VEGF 受体 1 的表达,并促进单纯疱疹病毒感染后的角膜血管生成。
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Role of IL-17 and Th17 cells in herpes simplex virus-induced corneal immunopathology.IL-17 和 Th17 细胞在单纯疱疹病毒诱导的角膜免疫病理中的作用。
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Ocular neovascularization caused by herpes simplex virus type 1 infection results from breakdown of binding between vascular endothelial growth factor A and its soluble receptor.单纯疱疹病毒 1 型感染引起的眼部新生血管是由于血管内皮生长因子 A 与其可溶性受体结合的破坏。
J Immunol. 2011 Mar 15;186(6):3653-65. doi: 10.4049/jimmunol.1003239. Epub 2011 Feb 16.
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Corneal sensation and subbasal nerve alterations in patients with herpes simplex keratitis: an in vivo confocal microscopy study.单纯疱疹病毒性角膜炎患者的角膜知觉和基底神经改变:一项共聚焦显微镜活体研究。
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Selective changes in human corneal sensation associated with herpes simplex virus keratitis.单纯疱疹病毒性角膜炎患者角膜感觉的选择性变化。
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