The modulatory effect of IL-10 and IL-12 genes on immune cells and OVA-induced asthmatic mice

• Main Authors: Hsiao-Chiao Su, 蘇筱喬
• Other Authors: 李岳倫助理
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/80153149791803769908

碩士 === 臺北醫學大學 === 醫學科學研究所 === 96 === The T helper type 2 cells (Th2) play a curial role in the initiation of allergic asthma. Asthma is characterized by reversible airway obstruction, eosinophilic infiltration, airway remodeling, mucus hypersecretion and airway hyperresponsiveness. In our studies, we use IL-10 or IL-12 expessing adenoviral vector to observe whether combination treatment can suppress the airway inflammation of allergic asthma. Firstly, we applied the Ad-IL-10/IL-12 to the bone marrow derived dendritic cells (DCs) and found such modified DCs expressed increased surface makers of CD 80, CD 86 and MHC class II. These modified DCs drived activated CD4+ T cells to differiate to specific T cell line. These special T cells secreted high levels of IL-10 and IFN-γ and suppressed the proliferation of effector T cells through cell-cell contact rather than the cytokine mediation. In the in vivo experiments, Ad-IL-10/IL-12 infected DCs were injected into OVA-induced asthmatic animal model to investigate whether modified DCs could prevent the development of asthma. The data showed that modified DCs suppressed the development of airway hyper-responsiveness, reduced airway inflammation and enhanced the expression of IL-10 and IFN-γ. We suggest that Ad-IL-10/IL-12 infected DCs can prevent the rise of asthma effectively. In addition, this modified DCs applied to the established asthmtic animal model and the same therapeutic effect was observed. In conclusion, we suggest that Ad-IL-10/IL-12 infected DCs induce a group of IL-10+ and IFN-γ+ T cells in vivo and such specific T cells can suppress the airway inflammation of asthmatic animal. Thus, such modified DCs may provide a more appropriate tool in future application of gene therapy for allergic diseases.