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

我们首先在我们的模型系统中证实了Th2免疫反应的抑制作用。LDV感染小鼠模型能稳定抑制各种Th2免疫反应，如嗜酸性粒细胞和免疫球蛋白的产生。我们在这个模型系统中检测了宿主对线虫寄生虫的免疫反应。肠道杯状细胞数量的动态变化与蠕虫数量成反比。接下来，我们研究了CD4^+T细胞(Th2细胞因子的来源)缺陷模型中肠道杯状细胞的粘蛋白的数量和性质，该模型不能驱逐巴西奈瑟氏菌。虽然巴西奈瑟氏菌感染可诱导杯状细胞产生岩藻糖和唾液酸链粘蛋白，但CD4~+T细胞缺陷模型不能产生这些粘蛋白。然而，注射重组IL-13可恢复唾液酸链粘蛋白的产生和驱虫作用。此外，在正常小鼠体内注射重组IL-13可诱导酸性连接粘蛋白，但对STAT-6缺陷小鼠无此作用。因此，IL-13介导的肠道杯状细胞的生长和唾液酸连接粘蛋白的产生是驱除巴氏新月形吸虫必不可少的因素，而IL-13的作用依赖于Stat-6的信号转导。

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.