Department of Immunology, Uppsala University, Uppsala, Sweden.
Curr Opin Endocrinol Diabetes Obes. 2013 Apr;20(2):118-23. doi: 10.1097/MED.0b013e32835edb89.
Type 1 diabetes (T1D) research is at present in a critical period of development and during the past few years several large phase III studies targeting T-cell autoimmunity in recent-onset patients with T1D failed to reach the primary endpoint.
Cause and pathogenesis of T1D remain largely unknown. In humans, insulitis is discrete, affects few islets and is present only in about one-third of patients with recent-onset T1D. The rapid increase in incidence of T1D argues against a decisive role for genetic factors and instead for the hypothesis that infectious agents, possibly entering the pancreas via the ductal compartment, are involved in disease pathogenesis. Repeated episodes of bacteria or virus-induced innate inflammations affecting only certain lobes of the pancreas fit well with the reported heterogeneity of the disease within the pancreas as well as with the slow progression over many years.
In humans there is limited support for T1D being primarily an autoimmune disease; instead available findings support the view that T1D can be regarded as an innate inflammatory disease affecting the entire pancreas, but with its main clinical manifestations emanating from the loss of the insulin-producing cells.
1 型糖尿病（T1D）的研究目前正处于关键的发展阶段，在过去几年中，几项针对 T1D 发病初期患者 T 细胞自身免疫的大型 III 期研究未能达到主要终点。
T1D 的病因和发病机制仍知之甚少。在人类中，胰岛炎是离散的，仅影响少数胰岛，并且仅存在于大约三分之一的 T1D 发病初期患者中。T1D 发病率的快速上升表明遗传因素不是决定性因素，而是感染因子可能通过导管腔进入胰腺参与疾病发病机制的假说。反复发生的细菌或病毒诱导的先天炎症仅影响胰腺的某些叶，这与胰腺内疾病的异质性以及多年来的缓慢进展非常吻合。
在人类中，T1D 主要是一种自身免疫性疾病的观点得到的支持有限；相反，现有发现支持 T1D 可被视为一种影响整个胰腺的先天炎症性疾病，但主要临床表现源自胰岛素产生细胞的丧失。
