Analysis of the host Th2 related immno-effector cell against the parasite

宿主 Th2 相关免疫效应细胞针对寄生虫的分析

• 批准号: 11660296
• 负责人: MORIMOTO Masahiro
• 金额: $ 2.3万
• 依托单位: Yamaguchi University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1999
• 资助国家: 日本
• 起止时间: 1999 至 2001
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-11660296/
• 关键词: Th2 (helper 2); goblet cell; Stat-6; mucin; lectin staining; IL-13; LDV infection; Nippostrongylus brasiriensis; Th2(Tヘルパー2); マスト細胞; 好酸球; IgE; GALT; aly; Th1(Tヘルパー1); マクロファージ; エフェクター細胞

We confirmed the suppressive effect of Th2 immuno-responses in our model system first. LDV infected mice model suppresses each Th2 immuno-responses, such as eosinophil and lgE production, stably. We examined host immuno-responses against nematode parasite Nippostrongylus brasiriensis in this model system. The kinetics of number of intestinal goblet cells is in inverse proportion to the number of worms. We next examined the number and the properties of mucin of intestinal goblet cells in CD4^+T cell (source of Th2 cytokines)-deficient models, which can not expel N. brasiriensis. Although N. brasiriensis infection induced fucose and sialic acid linkage mucin in goblet cell, CD4^+T cell-deficient models can not produce these mucins. However, injection of recombinant IL-13 restored production of sialic acid linkage mucin and worm expulsion. In addition, injection of recombinant IL-13 into normal mice induces acid linkage mucin, but not in stat-6 deficient mice.Thus, IL-13 mediated growth of intestinal gobket cell and production of sialic acid linkage mucin are essential for the expulsion of N. brasiriensis, and effect of IL-13 is depend on the signaltransduction of Stat-6.

我们首先在我们的模型系统中证实了Th 2免疫应答的抑制作用。LDV感染小鼠模型稳定抑制各种Th 2免疫反应，例如嗜酸性粒细胞和lgE产生。我们研究了宿主对线虫寄生虫巴西日本圆线虫在这个模型系统的免疫反应。肠道杯状细胞数量的动态变化与蠕虫数量成反比。接下来，我们检测了不能排出N的CD 4 ^+T细胞（Th 2细胞因子的来源）缺陷模型中肠杯状细胞粘蛋白的数量和性质。巴西人虽然N.巴西利亚感染诱导杯状细胞中岩藻糖和唾液酸连接的粘蛋白，CD 4 ^+T细胞缺陷模型不能产生这些粘蛋白。然而，注射重组IL-13恢复了唾液酸连接粘蛋白的产生和蠕虫排出。另外，IL-13可诱导正常小鼠产生酸性连接粘蛋白，而stat-6缺陷小鼠则无此作用，因此IL-13介导的小肠杯状细胞生长和唾液酸连接粘蛋白的产生是N.而IL-13的作用是通过Stat 6的信号转导来实现的。

项目成果

Morimoto M, Iwata H, and Hayashi T: "Lactic dehydrogenase virus infection inhibits allergic eosinophil reacion and IL-5 gene expression in vivo"Int. Arch. Allergy Immunol. 120. 78-84 (1999)

Morimoto M、Iwata H 和 Hayashi T：“乳酸脱氢酶病毒感染抑制体内过敏性嗜酸性粒细胞反应和 IL-5 基因表达”Int。

M Morimoto: "Lactic dehydrogenase virus(LDV)infection inhibits allergic eosinophil reaction in the airway"Research in Veterinary Science. (in press).

M Morimoto：“乳酸脱氢酶病毒（LDV）感染抑制气道中的过敏性嗜酸性粒细胞反应”兽医科学研究。

M Morimoto: "Lactic dehydrogenase virus infection reduces the explusion of the nematode Nippostrongylus brasiriensis"Parasitol.Res.. (in press).

M Morimoto：“乳酸脱氢酶病毒感染减少了巴西圆线虫的排除”Parasitol.Res..（正在出版）。

Morimoto M, Yamamoto M, and Hayashi T: "Lactic dehydrogenase virus infection reduces the explusion of the nematode Nippostrongylus brasiliensis"Parasitol. Res. (in press).

Morimoto M、Yamamoto M 和 Hayashi T：“乳酸脱氢酶病毒感染减少了巴西圆线虫的排除”寄生虫。

M Morimoto: "Lactic dehydrogenase virus infection inhibits allergic eosinophil reaction and IL-5 gene expression in vivo"Int.Arch.Allergy Immunol.. 120. 78-84 (1999)

M Morimoto：“乳酸脱氢酶病毒感染抑制体内过敏性嗜酸性粒细胞反应和IL-5基因表达”Int.Arch.AllergyImmunol..120.78-84(1999)