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一种新型特应性皮炎小鼠模型,通过经皮过敏原诱导形成 T 辅助细胞 2(Th2)极化。

A novel mouse model of atopic dermatitis that is T helper 2 (Th2)-polarized by an epicutaneous allergen.

机构信息

Department of Stem Cell and Regenerative Biology, Konkuk University, 120 Neungdongro, Gwangjin-gu, Seoul 05029, Republic of Korea.

School of Medicine, Konkuk University, 120 Neungdongro, Gwangjin-gu, Seoul 143-701, Republic of Korea.

出版信息

Environ Toxicol Pharmacol. 2018 Mar;58:122-130. doi: 10.1016/j.etap.2017.12.025. Epub 2017 Dec 29.

DOI:10.1016/j.etap.2017.12.025
PMID:29329020
Abstract

The pathogenesis of atopic dermatitis (AD) involves T helper 2 (Th2) cells, and effective therapies remain elusive due to the paucity of animal models. We aimed to develop a mouse model of an immune system aberration caused by allergen. Experiments were conducted in two phases. In experiment 1, BALB/c mice were sensitized with one of four chemical allergens - toluene diisocyanate (TDI), hexamethylene diisocyanate (HDI), trimellitic anhydride (TMA), or 2,4-dinitrochlorobenzene (DNCB) - for 3 weeks. Based on results of experiment 1, immunological features were compared between TMA-sensitized BALB/c mice and NC/Nga mice, after exposure to mite extracts, harmful chemicals and detergents in experiment 2. Sensitization by allergen caused a large number of pathological changes in the skin, and an increase in mast cell number. TMA-sensitized BALB/c mice models showed higher sensitivity to an environmental allergen than NC/Nga mice did. Overall, the initial sensitization with TMA leads to disturbances in Th2-mediated immunity.

摘要

特应性皮炎(AD)的发病机制涉及 T 辅助细胞 2(Th2),由于缺乏动物模型,有效的治疗方法仍然难以实现。我们旨在开发一种由过敏原引起的免疫系统异常的小鼠模型。实验分为两个阶段进行。在实验 1 中,BALB/c 小鼠用四种化学过敏原中的一种进行致敏 - 甲苯二异氰酸酯(TDI)、六亚甲基二异氰酸酯(HDI)、均苯四甲酸酐(TMA)或 2,4-二硝基氯苯(DNCB)- 持续 3 周。基于实验 1 的结果,在实验 2 中比较了 TMA 致敏的 BALB/c 小鼠和 NC/Nga 小鼠暴露于螨虫提取物、有害化学品和清洁剂后的免疫学特征。过敏原致敏导致皮肤大量病理变化,并增加肥大细胞数量。TMA 致敏的 BALB/c 小鼠模型对环境过敏原的敏感性高于 NC/Nga 小鼠。总的来说,初始的 TMA 致敏导致 Th2 介导的免疫紊乱。

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