Defective response to bacteria through lectin-type receptors in dendritic cells from Crohn diseases

克罗恩病树突状细胞中凝集素型受体对细菌的反应有缺陷

• 批准号: 18590701
• 负责人: OKAMOTO Susumu
• 金额: $ 2.49万
• 依托单位: Keio University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2006
• 资助国家: 日本
• 起止时间: 2006 至 2007
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-18590701/
• 关键词: Crohn; dendritic cells; lectin; sugar chain

Human peripheral blood monocytes were differentiated into three types of cells, that is, M-CSF-derived macrophages, GM-CSF-macophages, and dendritic cells. First we compared surface markers on these cells among normal controls (NL), ulcerative colitis (UC), and Crohn's disease (CD) patients, but could not demonstrate any difference in DC-SIGN (CD209), CD14, CD33, CD80, CD86, CD83, HLA-DR, CD206. Next, we stimulated these cells to measure cytokines with LPS and/or DC-SIGN ligands such as mannnann, zymosan, and laminarin. Dendritic cells tended to produce more IL-12 and IL-23, but there were no difference with statistical significance among NL, UC, and CD. Some previous reports demonstrated that DC-SIGN ligands could suppress the production of pro-inflammatory cytokines from LPS-stimulated macrophages. However, I could not see the suppressive effect of DC-SIGN ligands in this set of experiments and now I am trying to find optimal conditions.

人外周血单核细胞分化为三种类型的细胞，即M-CSF衍生的巨噬细胞，GM-CSF-噬菌体和树突状细胞。首先，我们比较了正常对照组（NL），溃疡性结肠炎（UC）和克罗恩病（CD）患者的表面标记，但在DC-SIGN（CD209），CD14，CD33，CD33，CD80，CD86，CD86，CD83，CD83，CD83，HLA-DR，HLA-DR，CD206中无法证明任何差异。接下来，我们刺激了这些细胞，以测量LPS和/或DC-SIGN配体（例如Mannnann，Zymosan和Laminarin）的细胞因子。树突状细胞倾向于产生更多的IL-12和IL-23，但在NL，UC和CD之间没有统计学意义没有差异。以前的一些报道表明，直流符号配体可以抑制来自LPS刺激的巨噬细胞的促炎性细胞因子的产生。但是，在这组实验中，我看不到DC-SIGN配体的抑制作用，现在我正在尝试找到最佳条件。