Development of a new therapy for Crohn's disease by using immuno-regulatory function of NOD2

利用NOD2的免疫调节功能开发克罗恩病新疗法

• 批准号: 21590532
• 负责人: WATANABE Tomohiro
• 金额: $ 2.91万
• 依托单位: Kyoto University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2009
• 资助国家: 日本
• 起止时间: 2009 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-21590532/
• 关键词: クローン病; NOD2; TLR; 粘膜免疫

Healthy gut mucosa exhibit tolerogenic responses to intestinal microflora. Excessive immune-reactions against intestinal microflora lead to the development of inflammatory bowel diseases. Mutations in NOD2 are associated with the development of Crohn's disease. Elucidation of mechanisms by which NOD2 mutations cause Crohn's disease provides new insights in the pathogenesis of colitis. Here we show that NOD2 activation inhibits both NF-. B activation and type I IFN production mediated by TLRs.

健康的肠道粘膜对肠道微生物群表现出耐受性反应。针对肠道菌群的过度免疫反应会导致炎症性肠病的发生。 NOD2 突变与克罗恩病的发生有关。阐明 NOD2 突变导致克罗恩病的机制为结肠炎的发病机制提供了新的见解。在这里，我们表明 NOD2 激活同时抑制 NF-。 TLR 介导的 B 激活和 I 型 IFN 产生。

项目成果

NOD1 contributes to mouse host defense against Helicobacter pylori viaindution of type I IFN and activation of the ISGF3 signaling pathway

NOD1 通过诱导 I 型 IFN 和激活 ISGF3 信号通路，有助于小鼠宿主防御幽门螺杆菌

• 发表时间: 2010
• 期刊: Journal of Clinical Investigation (in press)
• 作者: Watanabe Tomohiro;et al.
• 通讯作者: et al.

Activation of type I IFN signaling by NOD1 mediates mucosal host defense against Helicobacter pylori infection

• DOI: 10.4161/gmic.2.1.15162
• 发表时间: 2011-01
• 期刊: Gut Microbes
• 影响因子: 12.2
• 作者: Tomohiro Watanabe;N. Asano;A. Kitani;I. Fuss;T. Chiba;W. Strober