ROLE OF TH2 CELLS IN EOTAXIN REGULATION

哮喘是一种气道炎症疾病，其中气道嗜酸性粒细胞增多是一个突出的组织学特征。嗜酸性粒细胞可以释放有毒介质、脂质和促炎细胞因子，诱导气道高反应性。因此，确定将嗜酸性粒细胞招募到损伤部位的机制对于理解疾病的发病机制至关重要。趋化因子是一个分泌蛋白家族，在引导不同类型的白细胞到达组织损伤感染部位方面起着关键作用。本研究的目的是研究Th2细胞在调节嗜酸性粒细胞特异性趋化因子eotaxin表达中的作用。我们希望鉴定和表征Th2细胞释放的在mRNA和蛋白水平上影响eotaxin表达的分子或因子。然后，我们希望确定在促进eotaxin基因表达中重要的转录因子。这些分子的重要性将在体内使用现有的敲除动物进行检验。这项工作将有助于更好地了解Th2细胞和eotaxin哮喘的作用。

Asthma is a disease of airway inflammation in which airway eosinophilia is a prominent histologic feature. Eosinophils can release toxic mediators, lipids and pro-inflammatory cytokines that can induce airway hyper- responsiveness. Identifying the mechanisms that are involved in recruiting eosinophils to the site of injury are therefore critical in the understanding of pathogenesis of disease. Chemokines are a family of secreted proteins that play a critical role in directing different types of leukocytes to the site of infection of tissue damage. The aim of this proposal is to examine the role of Th2 cells in regulating the expression of eotaxin, a chemokine specific for eosinophils. We hope to identify and characterize molecules or factors released from Th2 cells that are responsible for affecting the expression of eotaxin at the mRNA and protein levels. We then hope to identify transcription factors that are important in promoting gene expression of eotaxin. The importance of these molecules will be examined in vivo using existing knockout animals. This work will lead to the greater understanding of the role of Th2 cells and eotaxin asthma.