The role of toll-like receptor 3 in chronic contact hypersensitivity induced by repeated elicitation
The role of toll-like receptor 3 in chronic contact hypersensitivity induced by repeated elicitation
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DOI：
10.1016/j.jdermsci.2017.07.017
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发表时间：
2017-11-01
影响因子：
4.6
通讯作者：
Katoh, Norito
中科院分区：
文献类型：
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作者：
Yasuike, Risa;Tamagawa-Mineoka, Risa;Katoh, Norito
背景：越来越多的证据表明，Toll样受体(Toll-like Receptor，TLR)-3信号参与了非感染性免疫和炎症反应以及病毒感染。特应性皮炎(AD)患者的皮肤常被病毒和细菌感染，导致特应性症状加重。目的：探讨TLR3在类似AD的慢性接触性超敏反应中的作用。方法：采用野生型(WT)和Toll样受体3基因敲除(TIR3KO)小鼠，通过反复应用半抗原、2，4，6-三硝基-1-氯苯(TNCB)或恶唑酮，在其耳部皮肤诱发慢性接触性超敏反应。结果：T1R3KO小鼠耳部肿胀较轻，皮肤、皮肤和皮肤中白细胞浸润较少。半抗原攻击后小鼠血清总IgE水平明显低于WT小鼠。T1R3KO小鼠耳部皮肤炎症细胞因子IL-33、IL-4、IL-10和干扰素-γ的表达水平也低于WT小鼠。结论：TLR3缺乏抑制了慢性接触性超敏反应的发生发展，提示TLR3信号可能参与了AD的发病机制。(C)2017年日本皮肤病研究学会。爱思唯尔爱尔兰有限公司出版。版权所有。
Background: Accumulating evidence suggests that Toll-like receptor (TLR)-3 signaling is involved in noninfectious immune and inflammatory reactions as well as in viral infections. The skin of patients with atopic dermatitis (AD) is often infected with virus and bacteria, leading to the aggravation of atopic symptoms. These findings suggest TLR3 signaling may be involved in the pathogenesis of AD, but the exact role of TLR3 in AD remains to be defined.Objective: The purpose of this study was to investigate the role of TLR3 in chronic contact hypersensitivity reactions induced by repeated elicitation, resembling the features of AD.Methods: Wild-type (WT) and Toll-like receptor 3 knockout (TIr3 KO) mice were sensitized, and chronic contact hypersensitivity reactions were elicited in their ear skin via repeated application of a hapten, 2,4,6-trinitro-1-chlorobenzene (TNCB) or oxazolone.Results: The T1r3 KO mice exhibited less ear swelling, less leukocyte infiltration into the skin, and lower serum total IgE levels than WT mice after hapten challenge. The T1r3 KO mice also displayed lower expression levels of inflammatory cytokines (interleukin (IL)-33, IL-4, IL-10, and interferon-gamma in their TNCB-treated ear skin than WT mice.Conclusion: These results showed that TLR3 deficiency suppressed the development of chronic contact hypersensitivity reactions, suggesting that TLR3 signaling may participate in the pathogenesis of AD. (C) 2017 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.