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研究揭示皮膚傷口愈合過程中的瘙癢產生機制
瀏覽: 發布日期:2020-07-18

本期文章:《免疫》:Online/在線發表

美國國立衛生研究院WanJun Chen課題組的一項最新發現表明,細胞因子TGF-β誘導真皮樹突狀細胞表達白介素31,從而激活感覺神經元并刺激傷口瘙癢。該項研究成果于2020年7月15日在線發表在《免疫》雜志上。

皮膚傷口愈合與瘙癢的不適感有關。研究人員揭示了這種瘙癢的潛在機制,并集中在愈合過程中釋放的可溶性因子。研究人員在瘙癢反應高峰期的皮膚傷口組織中發現大量白細胞介素31(IL-31)。 Il31-/-小鼠缺乏傷口誘導的瘙癢反應。IL-31由招募到傷口的皮膚傳統2型樹突狀細胞(cDC2)釋放,并增加了瘙癢感覺神經元的敏感性。

 

從晚期傷口分離的cDC2轉移到健康皮膚中足以誘導瘙癢,且依賴于IL-31表達。在體外向皮膚DC中添加促進傷口愈合的細胞因子TGF-β1足以誘導Il31表達,并且Tgfbr1f/f CD11c-Cre小鼠在體內傷口中顯示出抓撓的減少以及Il31表達的降低。

 

因此,cDC2在傷口愈合期間通過TGF-β-IL-31軸促進皮膚瘙癢,這可能對于傷口瘙癢有治療意義。

 

附:英文原文

Title: The Cytokine TGF-β Induces Interleukin-31 Expression from Dermal Dendritic Cells to Activate Sensory Neurons and Stimulate Wound Itching

Author: Junji Xu, Peter Zanvit, Lei Hu, Pang-Yen Tseng, Na Liu, Fu Wang, Ousheng Liu, Dunfang Zhang, Wenwen Jin, Nancy Guo, Yichen Han, Jessica Yin, Alexander Cain, Mark A. Hoon, Songlin Wang, WanJun Chen

Issue&Volume: 2020-07-15

Abstract: Cutaneous wound healing is associated with the unpleasant sensation of itching. Here we investigated the mechanisms underlying this type of itch, focusing on the contribution of soluble factors released during healing. We found high amounts of interleukin 31 (IL-31) in skin wound tissue during the peak of itch responses. Il31/ mice lacked wound-induced itch responses. IL-31 was released by dermal conventional type 2 dendritic cells (cDC2s) recruited to wounds and increased itch sensory neuron sensitivity. Transfer of cDC2s isolated from late-stage wounds into healthy skin was sufficient to induce itching in a manner dependent on IL-31 expression. Addition of the cytokine TGF-β1, which promotes wound healing, to dermal DCs in vitro was sufficient to induce Il31 expression, and Tgfbr1f/f CD11c-Cre mice exhibited reduced scratching and decreased Il31 expression in wounds in vivo. Thus, cDC2s promote itching during skin would healing via a TGF-β-IL-31 axis with implications for treatment of wound itching.

DOI: 10.1016/j.immuni.2020.06.023

Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30278-8

期刊信息

Immunity:《免疫》,創刊于1994年。隸屬于細胞出版社,最新if:21.522
官方網址:https://www.cell.com/immunity/home
投稿鏈接:https://www.editorialmanager.com/immunity/default.aspx

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