Deschamps I, Khalil I, Beressi J P, Hors J, Robert J J
INSERM U30, Hôpital des Enfants-Malades.
Ann Pediatr (Paris). 1991 Apr;38(4):205-10.
The mechanism of pancreatic beta-cell destruction in type I (insulin-dependent) diabetes mellitus (IDDM) involves autoimmune events directed against these cells. Anti-beta-cell autoimmunity occurs in genetically predisposed individuals and may precede clinical manifestations of IDDM by several years. Markers for beta-cell autoimmunity, especially islet-cell antibodies, are being used with increasing reliability both for detection of IDDM and for evaluating the risk of development of the disease. HLA alleles associated with IDDM include DR3 and DR4, with the risk of IDDM being especially high in individuals with the heterozygous combination DR3/DR4. Recent advances in molecular biology have resulted in more accurate identification of genetic variants and even of amino acid sequences associated with IDDM. These markers can be used to identify patients with genetic susceptibility to the disease. The mechanism of action of genes associated with IDDM is as yet unknown but probably involves the receptor function of HLA molecules for antigens during immune responses.
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针对这些细胞的自身免疫事件。抗β细胞自身免疫发生在具有遗传易感性的个体中，可能在IDDM临床表现出现前数年就已存在。β细胞自身免疫的标志物，尤其是胰岛细胞抗体，在检测IDDM以及评估该病发生风险方面的应用可靠性越来越高。与IDDM相关的HLA等位基因包括DR3和DR4，DR3/DR4杂合组合的个体患IDDM的风险特别高。分子生物学的最新进展使得能够更准确地识别与IDDM相关的基因变异甚至氨基酸序列。这些标志物可用于识别对该病具有遗传易感性的患者。与IDDM相关基因的作用机制尚不清楚，但可能涉及免疫反应期间HLA分子对抗原的受体功能。
