Department of Immunobiology, King's College London, School of Medicine and National Institute of Health Research Biomedical Research Centre at Guy's & St Thomas' NHS Foundation Trust and King's College, London, UK.
Diabet Med. 2013 Feb;30(2):147-54. doi: 10.1111/dme.12085.
Following almost 30 years of intensive research, initiated by the observation that Type 1 diabetes development is associated with a characteristic pancreatic immune cell infiltrate, a picture is emerging of which of the diverse effector arms of the immune system are involved in β-cell destruction. Like any chronic pathology, there is considerable complexity, and our ability to model the disease is hampered by a lack of ready access to the target organ and limited longitudinal analyses. However, it seems that putative pathways can start to be ruled in and out, in part as a result of focused mechanistic studies that make use of new technologies, and in part through analysis of the outcomes of clinical trials of new agents aimed at halting the disease process. The picture that emerges suggests a pathway to prevention that may require combinations of therapeutic agents that target different aspects of the immune system and will need to be used with due attention to their risk-benefit profiles.
经过近 30 年的深入研究，人们最初观察到 1 型糖尿病的发展与特征性的胰腺免疫细胞浸润有关，由此逐渐揭示了免疫系统的多种效应臂参与了β细胞的破坏。与任何慢性病理一样，其中存在着相当大的复杂性，而且由于缺乏对目标器官的便捷获取途径和有限的纵向分析，我们对该疾病建模的能力受到了阻碍。然而，似乎可以开始排除或确定某些潜在途径，部分原因是利用新技术进行了有针对性的机制研究，部分原因是通过分析旨在阻止疾病进程的新型药物的临床试验结果。由此得出的结论表明，预防的途径可能需要联合使用针对免疫系统不同方面的治疗药物，并且需要适当注意其风险-收益比。
