Horwitz Bruce H
Department of Pathology, Brigham and Women's Hospital, and Division of Emergency Medicine, Children's Hospital, Boston, Massachusetts 02115, USA.
Inflamm Bowel Dis. 2007 Apr;13(4):490-500. doi: 10.1002/ibd.20098.
Abnormal response to enteric microflora is a critical factor driving bowel inflammation in patients with inflammatory bowel disease (IBD). Mice with genetically engineered mutations have played a central role in both formulating this hypothesis and elucidating the mechanism that normally protect the host from excessive inflammation within the bowel. One emerging theme is the importance of regulation within the innate immune system in protecting from microflora-driven pathology. In this review, I describe how genetically engineered mice have played a crucial role in shaping our conceptual understanding of pathways that regulate the development of chronic bowel inflammation, and furthermore, explore data derived from the study of genetically engineered mice that implicates the fundamental importance of regulation within the innate immune system in the control of this process.
对肠道微生物群的异常反应是驱动炎症性肠病（IBD）患者肠道炎症的关键因素。具有基因工程突变的小鼠在提出这一假设和阐明正常情况下保护宿主免受肠道内过度炎症影响的机制方面都发挥了核心作用。一个新出现的主题是先天免疫系统内的调节在预防微生物群驱动的病理过程中的重要性。在这篇综述中，我描述了基因工程小鼠如何在塑造我们对调节慢性肠道炎症发展途径的概念理解方面发挥了关键作用，此外，还探讨了来自基因工程小鼠研究的数据，这些数据表明先天免疫系统内的调节在控制这一过程中具有根本重要性。
