Okada S, Sato K, Miyai Y, Masaki Y, Higuchi T, Ogino Y, Ota Z
Third Department of Medicine, Okayama University Medical School, Japan.
Diabetologia. 1987 Nov;30(11):869-73. doi: 10.1007/BF00274796.
The role of complement in the pathogenesis of diabetes was studied in 31 Type 1 (insulin-dependent) diabetic children by assaying serum islet cell surface antibody, C3, C4 and serum complement-dependent antibody-mediated cytotoxicity. Nine of 21 islet cell surface antibody-positive children were within 5 months of disease onset and showed significantly lower serum C3 and C4 levels than either 1 year later or the remainder of the islet cell surface antibody-positive children at 6-12 months after disease onset. The overall trend of all islet cell surface antibody-positive diabetic children within 1 year of disease onset was toward increased serum C3 and C4 levels as the disease progressed. Serum C4 concentration and complement-dependent antibody-mediated cytotoxicity which showed an initial negative correlation were uncorrelated 1 year later. Four children who were initially strongly islet cell surface antibody-positive but negative 1 year later also exhibited significantly higher (p less than 0.05) mean serum C4 levels after 1 year. There was a significant decrease in complement-dependent antibody-mediated cytotoxicity when sera from the diabetic children were treated with either ethylene glycol tetra-acetic acid or ethylene diamine tetra-acetic acid. These data strongly suggest that complement-dependent antibody-mediated cytotoxicity induced by the classical complement pathway involving an islet cell surface antibody may play an important role in the pathogenesis of Type 1 diabetes.
通过检测血清胰岛细胞表面抗体、C3、C4以及血清补体依赖抗体介导的细胞毒性，对31例1型（胰岛素依赖型）糖尿病儿童补体在糖尿病发病机制中的作用进行了研究。21例胰岛细胞表面抗体阳性儿童中，有9例处于疾病发作5个月内，其血清C3和C4水平显著低于疾病发作1年后或疾病发作6 - 12个月时其余胰岛细胞表面抗体阳性儿童。疾病发作1年内所有胰岛细胞表面抗体阳性糖尿病儿童的总体趋势是随着疾病进展血清C3和C4水平升高。血清C4浓度与补体依赖抗体介导的细胞毒性最初呈负相关，1年后则无相关性。4例最初胰岛细胞表面抗体强阳性但1年后转为阴性的儿童，1年后其平均血清C4水平也显著升高（p小于0.05）。用乙二醇四乙酸或乙二胺四乙酸处理糖尿病儿童血清后，补体依赖抗体介导的细胞毒性显著降低。这些数据强烈表明，由涉及胰岛细胞表面抗体的经典补体途径诱导的补体依赖抗体介导的细胞毒性可能在1型糖尿病发病机制中起重要作用。
