Boitard C, Timsit J
INSERM U25, Hôpital Necker, Paris.
Ann Endocrinol (Paris). 1990;51(3-4):119-22.
Insulin-dependent diabetes is the direct consequence of an autoimmune reaction causing the destruction of the beta cells of the islets of Langerhans in the pancreas. The frequent association of diabetes with other diseases involving the immune system, the detection of circulating antibodies aimed at the islet cells, the occurrence of the disease in subjects with peculiar HLA antigens are as many arguments supporting the immunological hypothesis. The study of animal models of insulin-dependent diabetes (BB rats, NOD mice) now allows demonstrating the autoimmune process. The transient effectiveness of cyclosporin demonstrated in the human disease confirms these data. The prospects of transplantation of the pancreas, of islets or of islet cells in diabetic subjects to compensate for the insulin deficiency therefore raises the double immunological problem of allogenic rejection and of the risk of recurrence of the anti-islet autoimmune disease.
胰岛素依赖型糖尿病是一种自身免疫反应的直接后果，该反应导致胰腺中胰岛的β细胞被破坏。糖尿病与其他涉及免疫系统的疾病频繁关联、针对胰岛细胞的循环抗体的检测、具有特殊HLA抗原的受试者中该疾病的发生，这些都是支持免疫假说的论据。对胰岛素依赖型糖尿病动物模型（BB大鼠、非肥胖糖尿病小鼠）的研究现在能够证明自身免疫过程。环孢素在人类疾病中显示出的短暂有效性证实了这些数据。因此，在糖尿病患者中移植胰腺、胰岛或胰岛细胞以弥补胰岛素缺乏的前景引发了同种异体排斥和抗胰岛自身免疫疾病复发风险这两个双重免疫问题。
