• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Experimental Animals >Analysis of novel model for autoimmune diseases, Dcir-deficient mice that identified by transcriptome analysis of arthritis model mice
【24h】

Analysis of novel model for autoimmune diseases, Dcir-deficient mice that identified by transcriptome analysis of arthritis model mice

机译：通过关节炎模型小鼠的转录组分析鉴定的新型自身免疫性疾病模型，Dcir缺陷型小鼠

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Rheumatoid arthritis (RA) is a typical autoimmune disease, and one of the most serious medical problems affecting approximately 1% of the worldwide people. It has been reported that various molecules have combined role in the pathogenesis of RA, but the etiopathogenesis has not been elucidated completely and there are no any radical treatment. We have previously established two mouse models for RA, Human T cell leukemia virus type I (HTLV-I)-transgenic mice and Interleukin-1 receptor antagonist (IL-1Ra)-deficient mice, which both develop spontaneous autoimmune arthritis. Gene expression in these models was comprehensively analyzed using microarrays, and we identified C-type lectin receptors (CLRs) as an arthritis-related gene cluster. In order to confirm the involvement of CLRs to the pathogenesis of arthritis, we selected immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing dendritic cell immunorececptor (Dcir), and generated Dcir-deficient mice. Interestingly, aged Dcir-deficient mice spontaneously develop autoimmune diseases like human Ankylosing spondylitis and Sjogren syndrome associated with elevated autoantibodies. Moreover, Dcir-deficient mice showed a markedly exacerbated response to collagen-induced arthritis, which is experimental RA model, in even young age. These results suggest that Dcir has a crucial role in maintaining the homeostasis of the immune system and negatively regulate the development of autoimmune disease. The analysis of novel model for autoimmune diseases, Dcir-deficient mice provide new insights into the pathogenesis of autoimmune diseases and the development of new therapeutics.
机译：类风湿关节炎（RA）是一种典型的自身免疫性疾病，是影响全世界约1％人口的最严重的医学问题之一。据报道，各种分子在RA的发病机理中起着联合作用，但其病因尚未完全阐明，也没有任何根治方法。我们以前已经建立了两种RA小鼠模型：人类T细胞白血病病毒I型（HTLV-1）转基因小鼠和白介素1受体拮抗剂（IL-1Ra）缺陷小鼠，它们均会发展为自发性自身免疫性关节炎。使用微阵列对这些模型中的基因表达进行了全面分析，我们确定了C型凝集素受体（CLR）是与关节炎相关的基因簇。为了确认CLRs参与关节炎的发病机制，我们选择了基于免疫受体酪氨酸的抑制性基序（ITIM）的树突状细胞免疫受体（Dcir），并生成了Dcir缺陷型小鼠。有趣的是，年龄不足的Dcir缺陷小鼠自发发展出自身免疫性疾病，例如人类强直性脊柱炎和与自身抗体升高相关的Sjogren综合征。此外，缺乏Dcir的小鼠甚至在很小的年龄就表现出对胶原诱导的关节炎（实验性RA模型）的明显加重反应。这些结果表明，Dcir在维持免疫系统的动态平衡和负面调节自身免疫疾病的发展中具有至关重要的作用。 Dcir缺陷小鼠自身免疫疾病新模型的分析为自身免疫疾病的发病机理和新疗法的发展提供了新见解。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号