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感染小鼠模型稳定地抑制了各种Th2免疫反应，如嗜酸性粒细胞和lgE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力学与蠕虫数量成反比。接下来，我们研究了CD4^+T细胞（Th2细胞因子的来源）缺陷模型中肠杯状细胞粘蛋白的数量和特性，这些模型不能驱逐巴西奈瑟菌。虽然巴西奈瑟菌感染在杯状细胞中诱导了聚焦和唾液酸连锁粘蛋白，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可以恢复唾液酸链粘蛋白的产生和蠕虫的排出。此外，将重组IL-13注射到正常小鼠体内可诱导酸链粘蛋白，而在stat-6缺陷小鼠体内则不能。因此，IL-13介导的肠杯状细胞的生长和唾液酸连锁粘蛋白的产生是驱逐布拉氏乳杆菌的必要条件，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.