肠上皮细胞编码microRNAs在轮状病毒感染及肠道耐受中的作用与相关机制分析-免疫学专业论文.docxVIP

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肠上皮细胞编码microRNAs在轮状病毒感染及肠道耐受中的作用与相关机制分析-免疫学专业论文.docx

肠上皮细胞编码microRNAs在轮状病毒感染及肠道耐受中的作用与相关机制分析-免疫学专业论文

第三军医大学硕士学位论文 第三军医大学硕士学位论文 PAGE PAGE 4 of protein-coding genes by targeting cognate mRNAs for degradation or translational repression. The gene expression regulation of microRNAs is modest and fine-tuning, and has been demonstrated that miRNAs participate in various biological processes, including innate and adaptive immune responses. There is a growing amount of evidence that miRNAs play critical roles in intricate host-pathogen interaction networks, such as HCV and HIV infection, and the regulation of normal immune function and inflammation. The intestine is described as an immune privileged site where immunoregulatory mechanisms simultaneously defend against pathogens, yet preserve tissue homeostasis to avoid immune- mediated pathology in response to environmental challenges and need refined regulation. Thus, we postulated that, as a kind of matster gene expression regulator, miRNA encoded by cells of intestinal immune system must be involving in gut homeostasis and immuno balance. We focus on miRNA in IECs rather than other cells to explore their roles in gastrointestinal disease. A latest research is coincident with our hypothesis, they shows gut-specific deletion of Dicer1 abolishing the induction of RELMb, a key Th2 antiparasitic cytokine. Their results indicated that epithelial microRNAs mediate the mucosa-immune system crosstalk and playing important roles in gut mucosal immunity. Our interest is in exploring pathogenesis and immune mechanisms of gastrointestinal disease typically happened in infants, such as rotaviurs infection induced diarrhea and Necrotizing enterocolitis (NEC) . Also, we try to understand the cellular and molecular difference betweem immature and mature enterocytes. As discussed above, we carry out research in two models, rotavirus infecion and development-related intestinal inflammation. In part I of our research, Our results showed that when Dicer’s expression in infected cell was downregulated by siRNA, rotavirus production increas

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