A Multihit Model: Colitis Lessons from the Interleukin-10-deficient Mouse.
A Multihit Model: Colitis Lessons from the Interleukin-10-deficient Mouse.
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DOI：
10.1097/mib.0000000000000468
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发表时间：
2015-08
影响因子：
4.9
通讯作者：
Bleich A
中科院分区：
文献类型：
--
作者：
Keubler LM;Buettner M;Häger C;Bleich A
文章首次在线发表3七月2015复杂的机制正在拉动字符串启动炎症性肠病的发展。目前的证据表明，遗传易感性（多态性），环境因素和宿主微生物群的相互作用导致粘膜免疫系统的失调。在过去的几十年里，白细胞介素-10缺陷小鼠已经成为反映这种疾病多因素性质的极好模型。在这里，我们想详细回顾遗传因素，免疫方面的相互作用，特别是总结和讨论微生物群在炎症性肠病的白细胞介素-10缺陷小鼠模型中的作用，作为一个多击模型，有助于结肠炎的发展。
Article first published online 3 July 2015 Complex mechanisms are pulling the strings to initiate the development of inflammatory bowel disease. Current evidence indicates that an interaction of genetic susceptibilities (polymorphisms), environmental factors, and the host microbiota leads to a dysregulation of the mucosal immune system. In the past decades, the interleukin-10–deficient mouse has served as an excellent model to mirror the multifactorial nature of this disease. Here, we want to review in detail the interplay of the genetic factors, immune aspects, and especially summarize and discuss the role of the microbiota contributing to colitis development in the interleukin-10–deficient mouse model of inflammatory bowel disease as a multihit model.