Irritable bowel syndrome (IBS) is a chronic functional gastrointestinal disorder that is characterized by abdominal pain and an altered defecation pattern. It affects between 5 and 20% of the general population and can seriously impact quality of life. The pathophysiology of IBS is rather complex and multifactorial including, for example, altered signalling by the gut–brain axis, dysbiosis, abnormal visceral pain signalling and intestinal immune activation. The latter has gained particular interest in recent years, with growing insight into the bidirectional communication between the nervous system and the immune system. In this Review, we detail the current evidence suggesting that immune activation contributes to the pathology seen in patients with IBS and discuss the potential mechanisms involved. Moreover, we describe how immune mediators, particularly those released by mast cells, can directly activate or sensitize pain-transmitting nerves, leading to increased pain signalling and abdominal pain. Finally, we discuss the potential of interventions targeting immune activation as a new therapeutic strategy for patients suffering from IBS.

肠易激综合征 (IBS) 是一种慢性功能性胃肠道疾病，其特征是腹痛和排便方式改变。它影响了 5% 到 20% 的普通人群，并可能严重影响生活质量。IBS 的病理生理学相当复杂和多因素，包括，例如，肠-脑轴信号改变、生态失调、内脏疼痛信号异常和肠道免疫激活。近年来，随着对神经系统和免疫系统之间双向通信的深入了解，后者引起了特别的兴趣。在这篇综述中，我们详细介绍了当前证据表明免疫激活有助于 IBS 患者的病理学，并讨论了所涉及的潜在机制。此外，我们描述了免疫介质如何，尤其是肥大细胞释放的那些，可以直接激活或敏感传递疼痛的神经，导致疼痛信号增加和腹痛。最后，我们讨论了针对免疫激活的干预措施作为 IBS 患者新治疗策略的潜力。