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关于胰岛素依赖型(IDDM,Ⅰ型)糖尿病的病因已有许多的研究,可以说从临床表现特征到病理生理学方面已基本取得一致意见。即是说胰岛素的绝对缺乏以及其发病机制是和自家免疫体系有关。目前,对于引起胰岛素缺乏的自家免疫机制,世界上正在进行研究。特别是BB大白鼠和NOD小白鼠能够非常相似地模拟出人类Ⅰ型糖尿病病理的实验动物模型,正用以进行发病机制、预防和治疗方面的研究。但为什么只在胰岛β细胞出现特异性破坏呢?目前认为发病前就已有胰岛炎(insulitis),而且血中除有ICA(islet cell antibody,胰岛细胞抗体),或ICSA(isletcells surface antibody,胰岛细胞表面抗体)之外,尚有其他自家抗体存在并已得到证明。现又
There have been many studies on the etiology of insulin-dependent (IDDM, type I) diabetes mellitus. It can be said that there is basically agreement on the pathophysiology from the clinical features. That is the absolute lack of insulin and its pathogenesis is related to their own immune system. Currently, there is ongoing research in the world of an autoimmune mechanism that causes insulin deficiency. In particular, BB rats and NOD mice are able to mimic very similar animal models of the pathology of human type 1 diabetes and are being used to study pathogenesis, prevention and treatment. But why only in pancreatic β-cell specific damage? It is currently thought that before the onset of insulitis, and the blood in addition to ICA (islet cell antibody, islet cell antibody, or ICSA (isletcells surface antibody, islet Cell surface antibodies), there are other self-antibodies exist and have been proved. Now again