Cytokines produced by immune cells contribute to the development and perpetuation of inflammatory bowel disease (IBD), namely Crohn’s disease and ulcerative colitis, by regulating various aspects of the inflammatory response. Pro-inflammatory cytokines trigger chronic intestinal inflammation, tissue damage, carcinogenesis and perpetuation of disease and suppress the resolution of inflammation in IBD. The clinical success of antibodies that neutralize tumour necrosis factor (TNF) and the cytokine IL-12p40 in individuals with IBD has underscored this concept. Moreover, genetic and preclinical studies have emphasized the crucial role of IL-23 in IBD, leading to clinical approval of antibodies targeting this cytokine. Multiple studies have also investigated the administration of cytokines with assumed anti-inflammatory effects, but this approach has yet to show any real clinical benefit in individuals with IBD. Recent studies have targeted the cytokine network through the use of multi-cytokine blockers (for example, Janus kinase (JAK) inhibitors), IL-2-induced regulatory T cells or advanced combination therapies that use multiple cytokine blockers simultaneously (for example, anti-TNF along with anti-IL-23 antibodies). This Review will focus on our current understanding of how cytokines produced by innate and adaptive immune cells contribute to IBD pathogenesis and discuss how their modulation may inform future treatments for IBD.

免疫细胞产生的细胞因子通过调节炎症反应的各个方面，促进炎症性肠病（IBD）（即克罗恩病和溃疡性结肠炎）的发展和持续。促炎细胞因子引发慢性肠道炎症、组织损伤、癌变和疾病持续，并抑制 IBD 炎症的消退。中和肿瘤坏死因子 (TNF) 和细胞因子 IL-12p40 的抗体在 IBD 患者中的临床成功强调了这一概念。此外，遗传和临床前研究强调了 IL-23 在 IBD 中的关键作用，从而导致针对该细胞因子的抗体获得临床批准。多项研究还调查了具有假定抗炎作用的细胞因子的施用，但这种方法尚未显示出对 IBD 个体有任何真正的临床益处。最近的研究通过使用多细胞因子阻滞剂（例如 Janus 激酶 (JAK) 抑制剂）、IL-2 诱导的调节性 T 细胞或同时使用多种细胞因子阻滞剂的先进联合疗法（例如抗-TNF 以及抗 IL-23 抗体）。本综述将重点关注我们目前对先天性和适应性免疫细胞产生的细胞因子如何促进 IBD 发病机制的理解，并讨论它们的调节如何为未来的 IBD 治疗提供信息。