Nerup J, Lernmark A
Am J Med. 1981 Jan;70(1):135-41. doi: 10.1016/0002-9343(81)90420-4.
Genetic susceptibility, environmental factors and immune mechanisms are implicated in the pathogenesis and etiology of insulin-dependent diabetes mellitus. The onset of the disease is associated with a major loss of beta cells, and inflammatory cells may be seen in and around the islets of Langerhans. Insulin-dependent diabetes is often associated with autoimmune endocrinopathies. Antipancreatic cell-mediated autoimmunity is found predominantly in young patients with insulin-dependent diabetes of recent onset as are antibodies reactive with cytoplasmic components or cell surface determinants of islet cells. Antibodies reactive with live islet cells may mediate complement-dependent cytotoxicity. The antigen(s) in the islet cells remain(s) to be identified and characterized. Further studies will be necessary to determine whether autoimmunity is the cause of beta-cell destruction or whether it is a consequence of damages caused by exogenous agents in susceptible persons.
遗传易感性、环境因素和免疫机制与胰岛素依赖型糖尿病的发病机制和病因有关。该疾病的发作与β细胞的大量丧失有关,并且在胰岛及其周围可见炎症细胞。胰岛素依赖型糖尿病常与自身免疫性内分泌病相关。抗胰腺细胞介导的自身免疫主要见于近期发病的年轻胰岛素依赖型糖尿病患者,与胰岛细胞胞质成分或细胞表面决定簇反应的抗体也是如此。与活胰岛细胞反应的抗体可能介导补体依赖性细胞毒性。胰岛细胞中的抗原仍有待鉴定和表征。需要进一步研究以确定自身免疫是β细胞破坏的原因,还是易感人群中外源因素造成损害的结果。