伊米奎莫德
炎症
免疫学
免疫系统
银屑病
医学
TLR7型
先天免疫系统
Toll样受体
作者
Reiko Matsumoto,Teruki Dainichi,Soken Tsuchiya,Takashi Nomura,Akihiko Kitoh,Matthew S. Hayden,Ken J. Ishii,Mayuri Tanaka,Tetsuya Honda,Gyohei Egawa,Atsushi Otsuka,Saeko Nakajima,Kazuo Sakurai,Yoshikatsu Nakano,Takashi Kobayashi,Yukihiko Sugimoto,Kenji Kabashima
出处
期刊:JCI insight
[American Society for Clinical Investigation]
日期:2018-08-09
卷期号:3 (15)
被引量:38
标识
DOI:10.1172/jci.insight.121175
摘要
Epithelial cells are the first line of defense against external dangers, and contribute to induction of adaptive immunity including Th17 responses. However, it is unclear whether specific epithelial signaling pathways are essential for the development of robust IL-17-mediated immune responses. In mice, the development of psoriatic inflammation induced by imiquimod required keratinocyte TRAF6. Conditional deletion of TRAF6 in keratinocytes abrogated dendritic cell activation, IL-23 production, and IL-17 production by γδ T cells at the imiquimod-treated sites. In contrast, hapten-induced contact hypersensitivity and papain-induced IgE production were not affected by loss of TRAF6. Loss of psoriatic inflammation was not solely due to defective imiquimod sensing, as subcutaneous administration of IL-23 restored IL-17 production but did not reconstitute psoriatic pathology in the mutant animals. Thus, TRAF6 was required for the full development of IL-17-mediated inflammation. Therefore, epithelial TRAF6 signaling plays an essential role in both triggering and propagating IL-17-mediated psoriatic inflammation.
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