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.

诸如克罗恩氏病和溃疡性结肠炎等炎症性肠病（IBD）的特征是遗传易感宿主中肠道免疫细胞的失控活化。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治疗的需求。研究发现免疫细胞和致病性免疫细胞电路的改变是IBD黏膜炎症和组织破坏的关键驱动因素。有缺陷的肠道屏障和微生物营养不良会引起免疫细胞的这种积聚和局部活化，从而导致促炎性细胞因子环路覆盖了抗炎信号，并导致慢性肠道炎症。