牛津大学、纽卡斯尔大学和剑桥大学医院的研究人员在《新英格兰医学杂志》发表研究，揭示了炎症性肠病（IBD）的一个长期未解之谜1。该团队分析了超过4900名IBD患者的数据，发现约3.5%的患者体内存在一种能够中和关键抗炎蛋白白介素-10（IL-10）功能的有害抗体，而这种抗体在健康人群中未被检测到1。这一发现阐明了特定基因变异与严重IBD之间的病理联系，解决了困扰科学界长达30年的难题：基因变异HLA-DRB1*01:03通过促进产生干扰IL-10的抗体，从而导致患者患上严重的炎症性肠病1。
据研究估算，英国全国可能有15,000至20,000名IBD患者携带这种破坏免疫调节平衡的有害抗体1。这项研究的主要作者包括牛津大学的Holm Uhlig教授、纽卡斯尔大学的Sophie Hambleton教授和剑桥大学医院的Rainer Doffinger博士1。相关成果发表于2026年10月26日1。这一突破有望推动针对此类特定机制患者的精准血液检测以及靶向治疗方法的开发，为改善部分IBD患者的临床预后提供新的方向1。
Scientists from Oxford University, Newcastle University, and Cambridge University Hospitals NHS Foundation Trust have identified a critical mechanism underlying inflammatory bowel disease (IBD), resolving a scientific puzzle that has persisted for three decades 1. The study, published in the New England Journal of Medicine on October 26, 2026, reveals that autoantibodies in certain patients neutralize interleukin-10 (IL-10), a protein essential for controlling inflammation 1. This discovery explains the link between specific genetic variations and severe forms of the disease, offering new avenues for diagnosis and treatment 1.
The research team analyzed data from more than 4,900 IBD patients and found that approximately 3.5% of them produced antibodies that interfered with IL-10 function 1. These harmful antibodies were not detected in healthy individuals, highlighting their pathological role 1. Based on these findings, researchers estimate that between 15,000 and 20,000 patients across the United Kingdom may carry this antibody profile 1.
A key component of the breakthrough is the identification of how the HLA-DRB1*01:03 genetic variant contributes to disease severity 1. The study demonstrates that this mutation promotes the production of anti-IL-10 antibodies, thereby disrupting the body’s natural anti-inflammatory defenses 1. Led by Professor Holm Uhlig of Oxford University, Professor Sophie Hambleton of Newcastle University, and Dr. Rainer Doffinger of Cambridge University Hospitals, the team suggests that this insight will facilitate precise blood testing and targeted therapies for affected patients 1.
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