Deschamps I, Hors J, Robert J J
INSERM U30 et Service d'endocrinologie et de diabète de l'enfant, Hôpital des Enfants-Malades, Paris.
Schweiz Med Wochenschr. 1990 Jan 20;120(3):46-53.
The mechanism of pancreatic B-cell destruction in type I (insulin-dependent) diabetes (IDDM) involves autoimmune phenomena based on genetic predisposition. The mechanism of action of the susceptibility genes is probably related to the function of the HLA molecules in the immune response. The genetic susceptibility is distinguished by increased frequency of the HLA antigens DR3 and DR4 and particularly their heterozygous combination DR3/DR4. Recent advances in molecular biology have resulted in a more precise definition of the genetic variants and corresponding amino acid sequences associated with IDDM. These markers may identify subjects at risk of developing the disease. However, the signs of islet-specific autoimmunity, e.g. islet-cell antibodies, which may be detected several years before the clinical onset of IDDM, are of greater predictive value. These and other arguments in favour of an autoimmune pathogenesis of type I diabetes have made preventive immunotherapy a goal for the future.
I型（胰岛素依赖型）糖尿病（IDDM）中胰腺β细胞破坏的机制涉及基于遗传易感性的自身免疫现象。易感基因的作用机制可能与HLA分子在免疫反应中的功能有关。遗传易感性的特征是HLA抗原DR3和DR4的频率增加，特别是它们的杂合组合DR3/DR4。分子生物学的最新进展使得与IDDM相关的基因变异和相应氨基酸序列的定义更加精确。这些标志物可以识别有患该病风险的个体。然而，胰岛特异性自身免疫的迹象，如胰岛细胞抗体，可在IDDM临床发病前数年检测到，具有更大的预测价值。这些以及其他支持I型糖尿病自身免疫发病机制的论据使预防性免疫疗法成为未来的一个目标。
