J Clin Invest. 2018 Nov 1;128(11):4758-4760. doi: 10.1172/JCI124303. Epub 2018 Oct 15.
The introduction of anti-TNF antibody therapy has changed the course of treatment for Crohn's disease. However, the fundamental mechanism for the onset of Crohn's disease is still unknown, and the treatment strategy for this disease remains suboptimal. The assessment of the disease phenotype based on key environmental factors and genetic background may indicate options for the personalized treatment of Crohn's disease. In this issue of the JCI, Liu et al. show that consumption of tobacco and the mutation of ATG16L1T300A, a prevalent Crohn's disease susceptibility allele, drive defects in cells at the bottom of the intestinal crypt, the Paneth cells. These factors may provide novel targets for personalized medicine.
抗 TNF 抗体治疗的引入改变了克罗恩病的治疗进程。然而,克罗恩病发病的根本机制仍不清楚,这种疾病的治疗策略仍然不尽人意。基于关键环境因素和遗传背景对疾病表型的评估可能为克罗恩病的个体化治疗提供选择。在本期 JCI 中,Liu 等人表明,吸烟和 ATG16L1T300A 突变(一种常见的克罗恩病易感等位基因)的消耗会导致肠隐窝底部的细胞(潘氏细胞)出现缺陷。这些因素可能为个体化医学提供新的靶点。