IL-23-和咪喹莫德诱导的实验性小鼠银屑病模型

Q2 Immunology and Microbiology
Tej Pratap Singh, Howard H. Zhang, Samuel T. Hwang, Joshua M. Farber
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引用次数: 26

摘要

全基因组关联研究发现,IL-23及其受体基因多态性在银屑病中很重要,阻断IL-23是治疗银屑病的有效方法。Aldara™是一种含有TLR7和TLR8激动剂咪喹莫特(IMQ)的乳膏,被发现可加重一些已有疾病患者的牛皮癣。皮内注射IL-23和局部应用Aldara/IMQ可诱导小鼠皮肤炎症,其特征与牛皮癣相似,包括表皮增生和表皮和真皮层炎症细胞的积累,这是由IL-17A、IL-22和其他与人类疾病有关的因素介导的。因此,这些模型可用于临床前研究,以研究银屑病的分子和细胞发病机制,以及评估潜在的治疗方法。本文提供了创建和评估IL-23和Aldara/ imq诱导的牛皮癣小鼠模型的详细方法。本文还提供了一种流式细胞术分析皮肤白细胞的方法。©2019 by John Wiley &儿子,Inc。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
IL-23- and Imiquimod-Induced Models of Experimental Psoriasis in Mice
Genome‐wide association studies have found that polymorphisms in genes for IL‐23 and its receptor are important in psoriasis, and blocking IL‐23 is an effective therapy in the disease. The use of Aldara™, a cream that contains the TLR7 and TLR8 agonist imiquimod (IMQ), was found to exacerbate psoriasis in some patients with pre‐existing disease. Intradermal injections of IL‐23 and topical application of Aldara/IMQ induce skin inflammation in mice with features similar to psoriasis—including epidermal hyperplasia and accumulation of inflammatory cells in epidermis and dermis—which is mediated by IL‐17A, IL‐22, and other factors implicated in the human disease. Consequently, these models can be used in preclinical studies to investigate the molecular and cellular pathogenesis of psoriasis, as well as in the evaluation of potential therapies. This article provides detailed methodologies for creating and evaluating the IL‐23‐ and Aldara/IMQ‐induced mouse models of psoriasis. The article also provides a protocol for analyzing skin leukocytes by flow cytometry. © 2019 by John Wiley & Sons, Inc.
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来源期刊
Current Protocols in Immunology
Current Protocols in Immunology Immunology and Microbiology-Immunology
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