University of Cambridge and Addenbrooke's Hospital, Gastroenterology Unit, Cambridge, UK. miles.parkes @ addenbrookes.nhs.uk
Dig Dis. 2012;30 Suppl 1:78-81. doi: 10.1159/000341130. Epub 2012 Oct 11.
Our appreciation of the genetic contribution to inflammatory bowel disease susceptibility has advanced substantially over the last 5 years, driven particularly by genome-wide association scanning but now complemented by a variety of other genomics technologies. We now have a much more detailed appreciation of the molecular genetic architecture of inflammatory bowel disease (IBD), and particularly the areas of overlap between Crohn's disease (CD) and ulcerative colitis (UC) (such as Th17 pathways) and the pathways which are disease-specific (such as NOD2 and autophagy for CD and the MHC and epithelial barrier genes for UC). The next steps will be to translate the new knowledge regarding pathways which are important in IBD pathogenesis into improved therapies and preventative strategies.
在过去的 5 年中，我们对炎症性肠病易感性的遗传贡献的认识有了很大的提高，这主要得益于全基因组关联扫描，但现在也有各种其他基因组学技术作为补充。我们现在对炎症性肠病（IBD）的分子遗传结构有了更详细的了解，特别是克罗恩病（CD）和溃疡性结肠炎（UC）之间的重叠区域（如 Th17 途径）和特定疾病的途径（如 CD 的 NOD2 和自噬以及 UC 的 MHC 和上皮屏障基因）。下一步将是将关于在 IBD 发病机制中起重要作用的途径的新知识转化为改进的治疗和预防策略。
