Mir-155通过肠道巨噬细胞IL-1信号通路活化Th-17调控DSS诱导的肠炎炎症

来源 :中国免疫学会第九届全国免疫学学术大会 | 被引量 : 0次 | 上传用户:jbdh2009
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背景:IBD是一种慢性炎症性肠病,威胁着全球百万以上人健康,其死亡率高,医疗费用昂贵.天然免疫和适应性免疫共同参与和控制IBD炎症,,肠道平衡的破坏是IBD发生的主要原因.Mir-155在多种炎性疾病中均上调,并证实其参与调控天然免疫和适应性免疫细胞的发育和功能.但迄今尚无有关Mir-155在IBD中调控天然免疫和适应性免疫细胞机制的研究.目的:本研究主要是探讨Mir-155调控DSS诱导的小鼠肠炎的分子机制
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细菌等病原体侵人体内后,可以被巨噬细胞吞噬消灭,也可以经巨噬细胞抗原提呈后启动适应性免疫应答.在巨噬细胞对病原体的免疫应答过程中巨噬细胞可以向不同的方向极化.在急性感染性疾病中,巨噬细胞以M1型极化为主,M1型巨噬细胞主要作用是促进炎症和杀灭细菌的作用;在慢性感染性疾病中,巨噬细胞以M2型极化为主,M2型巨噬细胞的主要作用是调节炎症.巨噬细胞的极化可以影响感染性疾病的发展,病原体也可以影响巨噬细胞
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研究背景:肺间质纤维化是一种慢性的、渐进的肺间质疾病,其特点是大量积累细胞外基质,重塑肺结构,并伴随着严重的关节炎等并发症.在肺间质纤维化发生发展过程中,巨噬细胞、Th17细胞及一些其他淋巴细胞都起到非常关键的作用.研究表明,在人或鼠的肺纤维化过程中,CD147的表达会上升,但是CD147在肺纤维化中的具体作用机制还不清楚.
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背景:据报道,快餐、零食等盐含量比正常家庭饮食可高100倍,其致病风险已经引起重视,但高盐对肠炎疾病的影响机制尚不明确.Th17细胞是高促炎细胞,能够诱导多种自身免疫病.IL-23可以通过诱导增加IL-23受体(IL-23R)的表达来促使初始T细胞分化为Th17,同时赋予Th17细胞致病功能.EAE小鼠模型证明,丝氨酸和苏氨酸转录调控因子SGK1是IL-23信号通路下游的一个重要节点.SGK1可以