Departments of Dermatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
Departments of Dermatology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, 465 Kajii-cho, Kawaramachi-Hirokoji, Kamigyo-ku, Kyoto, 602-8566, Japan.
J Dermatol Sci. 2017 Nov;88(2):184-191. doi: 10.1016/j.jdermsci.2017.07.017. Epub 2017 Aug 4.
Accumulating evidence suggests that Toll-like receptor (TLR)-3 signaling is involved in non-infectious 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.
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.
Wild-type (WT) and Toll-like receptor 3 knockout (Tlr3 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.
The Tlr3 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 Tlr3 KO mice also displayed lower expression levels of inflammatory cytokines (interleukin (IL)-33, IL-4, IL-10, and interferon-ɤ in their TNCB-treated ear skin than WT mice.
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.
越来越多的证据表明，Toll 样受体（TLR）-3 信号参与非传染性免疫和炎症反应以及病毒感染。特应性皮炎（AD）患者的皮肤经常受到病毒和细菌感染，导致特应症状加重。这些发现表明 TLR3 信号可能参与 AD 的发病机制，但 TLR3 在 AD 中的确切作用仍有待确定。
本研究旨在探讨 TLR3 在反复激发诱导的慢性接触性超敏反应中的作用，这种反应类似于 AD 的特征。
野生型（WT）和 Toll 样受体 3 敲除（Tlr3 KO）小鼠进行致敏，通过重复应用半抗原 2,4,6-三硝基-1-氯苯（TNCB）或恶唑酮在其耳部皮肤中诱发慢性接触性超敏反应。
与 WT 小鼠相比，在半抗原挑战后，Tlr3 KO 小鼠的耳部肿胀程度较小，皮肤白细胞浸润较少，血清总 IgE 水平较低。与 WT 小鼠相比，Tlr3 KO 小鼠在 TNCB 处理的耳部皮肤中炎症细胞因子（白细胞介素（IL）-33、IL-4、IL-10 和干扰素-ɤ）的表达水平也较低。
这些结果表明 TLR3 缺失抑制了慢性接触性超敏反应的发展，提示 TLR3 信号可能参与 AD 的发病机制。
