Cotto A, Gatti G, Calcamuggi G, Marcarino C, Emanuelli G
Minerva Med. 1981 Jan 28;72(3):129-40.
The incidence of immunological disorders seems to play a primary, significative role in the genesis of insulin-dependent diabetes mellitus (IDDM). Auto-immunological anti-pancreas alterations, both cell-mediated and humoral, have been detected in course of IDDM; moreover, the presence of antipancreatic antibodies seems to correlate with progressive destruction of islet cells and increased insulin deficiency. Animal models and human studies, revealing the pathologic entity of "insulitis", are consistent with an autoimmune component playing a part in the pathogenesis of diabetes mellitus. Furthermore, genotypic factors may be considered: recent studies prove the association between HLA system and IDDM; specifically, HLA antigens B8 and BW15 are found in significantly higher frequencies in juvenile onset insulin-dependent diabetics. Therefore, it can be hypothesized, in the pathogenesis of the disease, an altered immune response to an additional environmental diabetogenic factor; it has been postulated, on the ground of epidemiologic and experimental studies, the interference of a viral infection, that may act as a triggering event to pancreatic cell damage with a latent period of variable duration.
免疫紊乱的发生率似乎在胰岛素依赖型糖尿病（IDDM）的发病过程中起主要的、重要的作用。在IDDM病程中已检测到细胞介导和体液介导的自身免疫性抗胰腺改变；此外，抗胰腺抗体的存在似乎与胰岛细胞的进行性破坏和胰岛素缺乏增加相关。动物模型和人体研究揭示了“胰岛炎”的病理实体，这与自身免疫成分在糖尿病发病机制中起作用是一致的。此外，还可考虑基因型因素：最近的研究证实了HLA系统与IDDM之间的关联；具体而言，在青少年发病的胰岛素依赖型糖尿病患者中，HLA抗原B8和BW15的出现频率显著更高。因此，可以推测，在该疾病的发病机制中，对另一种环境致糖尿病因素的免疫反应发生了改变；基于流行病学和实验研究，有人提出病毒感染的干扰可能作为胰腺细胞损伤的触发事件，其潜伏期长短不一。
