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文章简介为了进一步解析肠道粘膜免疫反应中复杂的信号网络和肠道菌群免疫稳态之间的调控关系,研究团队利用IL-17A和FGF2基因缺陷小鼠建立的肠道炎症模型,多种免疫学分析手段和16SrRNA基因测序技术等方法,发现紊乱的肠道菌群除了会导致肠道的炎症反应以外,也会促使机体诱导Treg和Th17细胞分别产生FGF2和IL-17,来协同诱导肠道上皮层中损伤修复相关基因的表达,从而使得失调的肠道菌群和粘膜炎症反应回归稳态。FGF2或IL-17A基因的缺失将导致肠道上皮修复的
INTRODUCTION In order to further elucidate the regulatory relationship between the complex signaling networks in gut mucosal immune response and immune homeostasis in intestinal flora, the team used a model of intestinal inflammation established by IL-17A and FGF2 deficient mice, Immunological analysis and 16SrRNA sequencing technology and other methods found that disorganized intestinal flora in addition to causing intestinal inflammatory response, but also will induce the body to induce Treg and Th17 cells were generated FGF2 and IL-17, to co-induced intestinal The expression of damage-repair-related genes in the tract epithelial layer, so that the dysregulated intestinal flora and mucosal inflammation return to homeostasis. Deletion of the FGF2 or IL-17A gene will lead to intestinal epithelial repair