Charles M, Suzuki M, Sundsmo J, Waldeck N, Negishi K, Slater L, Ong K, Buckingham B, Kershnar A
Biomed Biochim Acta. 1984;43(5):615-9.
Data from our laboratory are reviewed showing that both cell-mediated cytotoxicity, complement-dependent antibody-mediated cytotoxicity, antibody-dependent cellular cytotoxicity, and complement-augmented antibody-dependent cellular cytotoxicity may provide mechanisms which kill pancreatic islets during pathogenesis of insulin-dependent (type I) diabetes. Xenogenic test systems employing dispersed rat islet target cells were employed. Most of the findings were reversible during clinical remission of diabetes.
我们实验室的数据回顾显示，细胞介导的细胞毒性、补体依赖的抗体介导的细胞毒性、抗体依赖的细胞毒性以及补体增强的抗体依赖的细胞毒性，都可能为胰岛素依赖型（I型）糖尿病发病机制中胰岛细胞的杀伤提供机制。采用了使用分散的大鼠胰岛靶细胞的异种测试系统。大多数研究结果在糖尿病临床缓解期是可逆的。
