Department of Systems Medicine, Gastroenterology, University of Rome "Tor Vergata" , Rome , Italy.
Expert Opin Biol Ther. 2019 Nov;19(11):1207-1217. doi: 10.1080/14712598.2019.1652267. Epub 2019 Aug 8.
: Although the etiology of inflammatory bowel diseases (IBD) remains unknown, accumulating evidence suggests that the intestinal tissue damage in these disorders is due to a dynamic interplay between immune cells and non-immune cells, which is mediated by cytokines produced within the inflammatory microenvironment. : We review the available data about the role of inflammatory cytokines in IBD pathophysiology and provide an overview of the therapeutic options to block the function of such molecules. : Genome studies, experiments with patients' samples and animal models of colitis, have largely advanced our understanding of how cytokines modulate the ongoing mucosal inflammation in IBD. However, not all the cytokines produced within the damaged gut seem to play a major role in the amplification and perpetuation of the IBD-associated inflammatory cascade. Indeed, while some of the anti-cytokine compounds are effective in some subgroups of IBD patients, others have no benefit. In this complex scenario, a major unmet need is the identification of biomarkers that can predict response to therapy and facilitate a personalized therapeutic approach, which maximizes the benefits and limits the adverse events.
虽然炎症性肠病(IBD)的病因仍然未知,但越来越多的证据表明,这些疾病中的肠道组织损伤是由于免疫细胞和非免疫细胞之间的动态相互作用引起的,这种相互作用是由炎症微环境中产生的细胞因子介导的。
我们回顾了关于炎症细胞因子在 IBD 病理生理学中的作用的现有数据,并提供了抑制这些分子功能的治疗选择概述。
基因组研究、患者样本实验和结肠炎动物模型在很大程度上提高了我们对细胞因子如何调节 IBD 中持续的黏膜炎症的理解。然而,并非所有在受损肠道中产生的细胞因子似乎都在放大和延续 IBD 相关炎症级联反应中发挥主要作用。事实上,虽然一些抗细胞因子化合物对某些 IBD 患者亚组有效,但其他化合物则没有益处。在这种复杂的情况下,一个主要的未满足的需求是确定能够预测对治疗反应的生物标志物,并促进个性化治疗方法,最大限度地提高益处并限制不良反应。