Targeting immune cell circuits and trafficking in inflammatory bowel disease
针对免疫细胞回路和炎症性肠病的贩运
摘要：
Inflammatory bowel diseases (IBDs) such as Crohn's disease and ulcerative colitis are characterized by uncontrolled activation of intestinal immune cells in a genetically susceptible host.Due to the progressive and destructive nature of the inflammatory process in IBD, complications such as fibrosis, stenosis or cancer are frequently observed, which highlights the need for effective anti-inflammatory therapy.Studies have identified altered trafficking of immune cells and pathogenic immune cell circuits as crucial drivers of mucosal inflammation and tissue destruction in IBD.A defective gut barrier and microbial dysbiosis induce such accumulation and local activation of immune cells, which results in a pro-inflammatory cytokine loop that overrides anti-inflammatory signals and causes chronic intestinal inflammation.This Review discusses pathogenic cytokine responses of immune cells as well as immune cell trafficking as a rational basis for new translational therapies in IBD.
诸如克罗恩病和溃疡性结肠炎的炎性肠病（IBD）的特征在于遗传易感宿主中肠免疫细胞的不受控制的激活。由于IBD中炎症过程的进行性和破坏性，经常观察到诸如纤维化，狭窄或癌症的并发症，这突出了对有效抗炎疗法的需要。研究已经确定免疫细胞和致病性免疫细胞回路的改变是IBD中粘膜炎症和组织破坏的重要驱动因素。肠道屏障和微生物生态失调导致免疫细胞的这种积累和局部活化，这导致促炎细胞因子环超越抗炎信号并引起慢性肠道炎症。该综述讨论了免疫细胞的致病细胞因子反应以及免疫细胞运输，作为IBD中新的翻译疗法的合理基础。
针对免疫细胞回路和炎症性肠病的贩运
摘要：
Inflammatory bowel diseases (IBDs) such as Crohn's disease and ulcerative colitis are characterized by uncontrolled activation of intestinal immune cells in a genetically susceptible host.Due to the progressive and destructive nature of the inflammatory process in IBD, complications such as fibrosis, stenosis or cancer are frequently observed, which highlights the need for effective anti-inflammatory therapy.Studies have identified altered trafficking of immune cells and pathogenic immune cell circuits as crucial drivers of mucosal inflammation and tissue destruction in IBD.A defective gut barrier and microbial dysbiosis induce such accumulation and local activation of immune cells, which results in a pro-inflammatory cytokine loop that overrides anti-inflammatory signals and causes chronic intestinal inflammation.This Review discusses pathogenic cytokine responses of immune cells as well as immune cell trafficking as a rational basis for new translational therapies in IBD.
诸如克罗恩病和溃疡性结肠炎的炎性肠病（IBD）的特征在于遗传易感宿主中肠免疫细胞的不受控制的激活。由于IBD中炎症过程的进行性和破坏性，经常观察到诸如纤维化，狭窄或癌症的并发症，这突出了对有效抗炎疗法的需要。研究已经确定免疫细胞和致病性免疫细胞回路的改变是IBD中粘膜炎症和组织破坏的重要驱动因素。肠道屏障和微生物生态失调导致免疫细胞的这种积累和局部活化，这导致促炎细胞因子环超越抗炎信号并引起慢性肠道炎症。该综述讨论了免疫细胞的致病细胞因子反应以及免疫细胞运输，作为IBD中新的翻译疗法的合理基础。
