Inflammatory bowel disease (IBD) is an autoimmune disease characterized by unresolved colitis and epithelial injury. Intestinal microbiota and its interaction with immune system are critical etiologic factors. In response to gut virome and bacteria derived nucleic acid, interferon regulatory factors (IRFs) are activated to promote the production of cytokines, including type I interferons (IFN-Is), to help maintain intestinal homeostasis under both physiological and pathophysiological conditions. However, derailed IRF/IFN-I pathway other-wisely contributes to the progression of IBD with distinct IRF member exerting differential regulatory effect. Here, we summarize the recent advances regarding the role of IRF/IFN-I pathway in the development of IBD. We emphasize that IFN-I is a double-edged sword in IBD pathogenesis, as IFN-Is are protective in acute colitis while becoming pro-inflammatory during the chronic recovery phase. Besides, the functional outcome of IRFs is diverse and complex, which hinges on the cell types affected and the presence of other immune mediators. All in all, IRF/IFN-I pathway serves as a versatile regulator in IBD pathogenesis and holds the potential for therapeutic interventions.

炎性肠病（IBD）是一种以自身免疫性疾病为特征的未解决的结肠炎和上皮损伤。肠道菌群及其与免疫系统的相互作用是关键的病因。响应肠道病毒和细菌衍生的核酸，干扰素调节因子（IRF）被激活以促进包括I型干扰素（IFN-Is）在内的细胞因子的产生，从而有助于在生理和病理生理条件下维持肠道稳态。但是，出轨的IRF / IFN-I途径在其他方面有助于IBD的进展，而独特的IRF成员发挥着不同的调节作用。在这里，我们总结了有关IRF / IFN-I途径在IBD发展中的作用的最新进展。我们强调IFN-I是IBD发病机理中的一把双刃剑，因为IFN-Is在急性结肠炎中具有保护作用，而在慢性恢复阶段却变得发炎。此外，IRF的功能结果是多种多样和复杂的，这取决于受影响的细胞类型和其他免疫介质的存在。总而言之，IRF / IFN-I途径可作为IBD发病机制中的多功​​能调节剂，具有治疗干预的潜力。