IMMUNOLOGY OF THE SCHISTOSOME EGG GRANULOMA

该项目包括T辅助细胞的细胞/分子分析， 亚群功能和炎症、调节信号的产生 它们参与了植物的进化， 曼氏血吸虫虫卵诱发的肉芽肿性炎症。 我们的远程 目的是阐明肉芽肿形成的机制， 设计免疫干预以改善肉芽肿病理 曼氏血吸虫病 研究目标分为 三个相互关联的领域：1。Th 1、Th 2范式与 肉芽肿形成。 重组细胞因子的免疫干预， 用抗细胞因子抗体检测感染小鼠体内的混合T 将响应子集设置为Th 1或Th 2模式。Stat-deficient和Th 1，Th 2细胞 注射小鼠建立Th 1或Th 2型肉芽肿模型 通过细胞因子mRNA表达（RT-PCR）或生产概况证实。 Th 1和NK细胞在肉芽肿诱导、抑制 亚群交叉调节，沿着趋化因子参与， 考察 2.血吸虫卵介导的内皮细胞活化。 卵抗原诱导内皮细胞活化，表达为粘附 分子展示、细胞因子分泌、增殖和血管生成 将在体外进行检查。 3.粘附分子的作用， 细胞外基质在肉芽肿演变、纤维化和退化中的作用。 膜粘附分子在白细胞相互作用中的作用， 阐明了肉芽肿演变和细胞外基质沉积 在抗体处理的或粘附分子缺陷的小鼠中。 的影响 Th 1、Th 2细胞对基质形成纤维化的作用及基质- 研究了T细胞活化或凋亡的衍生信号。

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.