S1PR3的缺失减轻了咪喹莫特银屑病模型小鼠的抓挠行为,但在MC903特应性皮炎模型中没有

Rose Z. Hill, Ziad Rifi, Cliff Vuong, D. Bautista
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引用次数: 3

摘要

在这里,我们研究鞘氨醇1-磷酸受体3 (S1PR3)在慢性瘙痒中的作用。我们使用2种小鼠模型-特应性皮炎的MC903模型和银屑病的咪喹莫特模型-来研究S1PR3对慢性瘙痒的贡献。我们测量了这些小鼠模型中S1PR3−/−、+/−和+/+动物的抓痕行为。虽然我们在MC903模型中没有观察到S1PR3缺失对瘙痒行为的影响,但在S1PR3−/−动物中,咪喹莫德诱发的瘙痒行为有所减少。总的来说,这些数据支持S1PR3信号在银屑病而非特应性瘙痒的发展中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Loss of S1PR3 attenuates scratching behaviors in mice in the imiquimod model of psoriasis, but not in the MC903 model of atopic dermatitis
Here we examine the role of sphingosine 1-phosphate receptor 3 (S1PR3) in chronic itch. We used 2 mouse models—the MC903 model of atopic dermatitis and the imiquimod model of psoriasis—to examine the contribution of S1PR3 to chronic itch. We measured scratching behaviors in these mouse models in S1PR3−/−, +/−, and +/+ animals. Whereas we observed no effect of loss of S1PR3 on itch behaviors in the MC903 model, imiquimod-evoked itch behaviors were reduced in S1PR3−/− animals. Overall, the data support a role for S1PR3 signaling in the development of psoriatic but not atopic itch.
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