IL-17在肺鼠疫中的免疫效应及其机制研究

肺鼠疫具有高度传染性，通常致命。基于肺鼠疫实验动物模型的研究进展，前期工作发现感染小鼠的肺泡灌洗液和肺组织中除IL-10和IL-6等促炎性因子分泌增高外，IL-17水平也明显增高。在肺泡灌洗液中浸润的炎症细胞（巨噬细胞、中性粒细胞和T细胞等）明显增多。IL-17A基因敲除小鼠实验显示，小鼠对肺鼠疫易感性增强。这提示IL-17在免疫细胞介导的肺鼠疫保护性防御效应中有重要调控作用。本课题将在深入探讨肺鼠疫感染中IL-17的免疫保护作用基础上，进一步研究其免疫细胞调控规律，并试图初步阐明其分子机制。该研究将首次阐明IL-17在肺鼠疫感染中调控效应。同时，该研究也将利用感染模型有助于深入探究IL-17介导的免疫细胞调控反应规律。

Pneumonic plague is a rapidly progressing and often-fatal disease. According to animal model research progresses in pneumonic plague, our previous studies show that there is significantly increased IL-17 other than proinflammatory cytokines IL-10 and IL-6 et al. in bronchoalveolar lavage fluid (BALF) of infected mice. Furthermore, there are increased inflammatory macrophages, neutrophils, and T cells infiltrated in local lung from BALF. Importantly, the death ratio could be increased in IL-17 knockout mice postinfection by plague. All these indicate IL-17 plays an immune protective effect against pneumonic plague. This study should further clarify the basic immune protective effects of IL-17 for pneumonic plague and immune modulatory regularities and primary molecular mechanisms. This study should firstly clarify the immune regulatory effects of IL-17 in pneumonic plague. Meanwhile, it should contribute to basic immunological theories about IL-17 and immune effects with an infected model.