IMMUNOLOGY OF THE SCHISTOSOME EGG GRANULOMA

该项目包括T辅助细胞的细胞/分子分析 子集功能和炎性调节信号的产生 参与进化、华丽的状态和进化的 S曼氏虫卵诱导的肉芽肿性炎症。我们的远距离飞行 目的：阐明肉芽肿的形成机制和发病机制。 设计免疫干预措施以改善肉芽肿病理 在曼氏血吸虫病中。研究目标分为 三个相互关联的领域：1.Th1、Th2范式与 肉芽肿形成。重组细胞因子的免疫干预， 抗细胞因子抗体被用来极化感染的小鼠的混合T细胞 子集响应进入Th1或Th2模式。STAT缺陷与Th1、Th2细胞 用注射的小鼠建立Th1型或Th2型肉芽肿模型 经细胞因子mRNA表达(RT-PCR)或产物谱证实。 Th1和NK细胞在肉芽肿诱导、抑制、 子集交叉调节，以及趋化因子的参与，是 检查过了。2.血吸虫卵介导的内皮细胞激活。 卵子抗原(S)诱导内皮细胞活化的黏附表达 分子展示、细胞因子分泌、增殖与血管生成 将在体外进行检测。3.黏附分子的作用和 细胞外基质在肉芽肿演变、纤维化和退变中的作用。 膜黏附分子在白细胞相互作用中的作用 肉芽肿演变和细胞外基质沉积的阐明 在抗体治疗或黏附分子缺陷小鼠中。影响 Th1、Th2细胞在基质形成纤维化中的作用 研究了T细胞激活或凋亡的衍生信号。

This project comprises the cellular/molecular analyses of T helper subset functions and the generation of inflammatory, regulatory signals that participate in the evolution, florid state and involution of the S mansoni egg-induced granulomatous inflammation. Our long range objective is to elucidate the mechanisms of granuloma formation and design immunologic interventions to ameliorate granulomatous pathology in schistosomiasis mansoni. The research objectives are divided into three interrelated areas: 1. Th1, Th2 paradigm and the polarization of granuloma formation. Immune interventions by recombinant cytokines, anti-cytokine abs are done to polarize in infected mice the mixed T subset response into Th1 or Th2 mode. Stat-deficient and Th1, Th2 cell injected mice are used to establish Th1 or Th2 type granuloma models confirmed by cytokine mRNA expression (RT-PCR) or production profile. The roles of Th1, and NK cells in granuloma induction, suppression, subset cross regulation, along with chemokine participation, are examined. 2. Schistosome eggs-mediated endothelial cell activation. Egg antigen(s) induced endothelial cell activation expressed by adhesion molecule display, cytokine secretion, proliferation and angiogenesis will be examined in vitro. 3. Role of adhesion molecules and extracellular matrix in granuloma evolution, fibrosis and involution. The role of membrane adhesion molecules in leukocyte interactions, granuloma evolution and extracellular matrix deposition is elucidated in antibody treated or adhesion molecule deficient mice. The influence of Th1, Th2 cells on matrix formation fibrosis and the role of matrix- derived signals on T cell activation or apoptosis are investigated.