Chauhan Gaurav, Rieder Florian
Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA; Department of Gastroenterology, Hepatology and Nutrition, Digestive Diseases Institute; Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195, USA.
Surg Clin North Am. 2025 Apr;105(2):201-215. doi: 10.1016/j.suc.2024.10.008. Epub 2024 Nov 26.
Inflammatory bowel diseases (IBDs) are relapsing, remitting inflammatory diseases of the intestinal tract. Familial aggregation and genome-wide association studies revealed susceptibility variants that point toward a combination of innate immune and adaptive immune dysregulation that in concert with environmental factors, such as our microbiome, can initiate and perpetuate inflammation. Innate immune perturbations include functional abnormalities in the intestinal barrier, endoplasmic reticulum stress, and abnormal recognition of microbes. Adaptive immune changes include dysregulation of cytokines, regulatory T cells, and leukocyte migration. IBD is linked with an abnormal wound-healing response leading to fibrosis. This article summarizes key pathogenic mechanisms in the pathogenesis of IBDs.
炎症性肠病(IBDs)是肠道的复发性、缓解性炎症性疾病。家族聚集性和全基因组关联研究揭示了一些易感变异,这些变异指向先天性免疫和适应性免疫失调的组合,这种失调与环境因素(如我们的微生物群)共同作用,可引发并持续炎症。先天性免疫紊乱包括肠道屏障功能异常、内质网应激以及对微生物的异常识别。适应性免疫变化包括细胞因子、调节性T细胞和白细胞迁移的失调。IBD与导致纤维化的异常伤口愈合反应有关。本文总结了IBD发病机制中的关键致病机制。