Ex Vivo Splenocyte Cytokine Expressions and Clinical Scores of Experimental Autoimmune Encephalomyelitis Mouse Treated with Dendritic Cell Modulated by Decoy Receptor 3

• Main Authors: Hsiu-Jung Lin, 林秀蓉
• Other Authors: Shu-Fen Wu
• Format: Others
• Language: en_US
• Published: 2009
• Online Access: http://ndltd.ncl.edu.tw/handle/70190782468744877452

碩士 === 國立中正大學 === 生命科學系暨分子生物研究所暨生物醫學研究 === 97 === It was previously indicated that Th1 cells were the pathogenic T cell in EAE. Recent studies indicated that Th17 cells also play important roles in pathogenesis of EAE. Naïve CD4 T cells differentiate, whatever Th1 or Th17 cells, into different subsets of T helper cells, they all need antigen-presenting cells – especially dendritic cells to present antigen, and different cytokine environments. In previous studies, DcR3-treated dendritic cells (DcR3-DC) can suppress both proliferation and interferon gamma secretion of CD4+ T cells in Th1 autoimmune diabetic model and human lymphocytes. To investigate whether DcR3 modulated DC can down-regulate Th17 population and inhibit the clinical score of EAE mice, we intravenously injected DcR3-DC into experimental mice before or after EAE induction, and record the EAE progress. As our results, DcR3-DC indeed prolonged the EAE progress and decreased EAE severity. It also significantly decreased splenocyte cytokine secretion , not only IL-17 but IL-2, 4, 6, 10, IFN-γ and TNF, compared with control DC in pre-treated and post-treated once experiments. Therefore, DcR3-DC may be useful for EAE prevention, or even therapy.