Investigation of IL-23/Th17 axis in pathogenesis of psoriasis using a mouse model.

使用小鼠模型研究 IL-23/Th17 轴在银屑病发病机制中的作用。

• 批准号: 22591242
• 负责人: TAKAISHI Mikiro
• 金额: $ 2.91万
• 依托单位: Kochi University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22591242/
• 关键词: 乾癬; モデルマウス; Th17; IL-23; IL-22; Stat3; IL-17; 乾癬; モデルマウス; Th17; IL-23; IL-22; Stat3; IL-17

The roles of IL-23 and IL-22 in pathogenesis of psoriasis were investigated using K5.Stat3C transgenic mice, as a unique mouse model for psoriasis. The development of psoriasis-like lesions was attenuated in the K5.Stat3C mice being deficient in IL-23 production. In other hands, the lesions in the IL-22 deficient mice were generated as same as in the control mice. The results indicated that IL-23 played a significant role in psoriasis and that some alternative pathways could compensate the loss of IL-22 in development of psoriasis-like lesions.

使用K5.STAT3C转基因小鼠作为牛皮癣的独特小鼠模型，研究了IL-23和IL-22在牛皮癣发病机理中的作用。牛皮癣样病变的发育在IL-23产生缺乏的K5.STAT3C小鼠中被衰减。在其他手中，IL-22缺乏小鼠中的病变与对照小鼠一样。结果表明，IL-23在牛皮癣中发挥了重要作用，并且某些替代途径可以补偿类似牛皮癣的病变发展中IL-22的损失。