Schröder D, Schmidt S, Klöting I, Hehmke B
Institute of Diabetes Gerhardt Katsch, Karlsburg of the Ernst-Moritz-Arndt-University of Greifswald, Germany.
Autoimmunity. 1993;14(4):283-9. doi: 10.3109/08916939309079230.
Diabetes-prone BB/OK rats aged 30 to 35 days were subjected to three sequential intrasplenic injections of unfractionated homogenate prepared from Langerhans' islets of newborn syngeneic BB/OK rats. Syngeneic islet antigen administration resulted in increased complement-dependent antibody-mediated cytotoxicity (C'AMC) to rat pancreatic islet cells in serum, compared to buffer-treated control animals as detected by 51Cr-release assay. However, the increase of anti-islet-cell cytotoxicity neither impaired glucose tolerance nor affected the incidence of diabetes and the age at manifestation. In contrast to BB/OK rats developing diabetes, animals remaining long-term normoglycaemic did not show an enhancement of cytotoxicity to islet cells within twelve days after the first islet antigen injection as revealed retrospectively. In conclusion, humoral mediated anti-islet-cell cytotoxicity is not decisively involved in pancreatic beta-cell destruction and promotion of diabetes development in BB/OK rats, but animals becoming diabetic seem to be characterized by a stronger immunological reactivity upon syngeneic islet antigen challenge as indicated by an increase of anti-islet C'AMC compared to long-term normoglycaemic rats.
将30至35日龄的糖尿病易感BB/OK大鼠，经脾内连续三次注射由同基因新生BB/OK大鼠胰岛制备的未分级匀浆。与经缓冲液处理的对照动物相比，通过51Cr释放试验检测发现，给予同基因胰岛抗原后血清中对大鼠胰岛细胞的补体依赖性抗体介导的细胞毒性（C'AMC）增加。然而，抗胰岛细胞细胞毒性的增加既未损害葡萄糖耐量，也未影响糖尿病的发病率及发病年龄。与发生糖尿病的BB/OK大鼠相反，回顾性研究发现，长期血糖正常的动物在首次注射胰岛抗原后12天内，对胰岛细胞的细胞毒性并未增强。总之，体液介导的抗胰岛细胞细胞毒性并非决定性地参与BB/OK大鼠胰腺β细胞的破坏及糖尿病的发展，但与长期血糖正常的大鼠相比，发生糖尿病的动物在受到同基因胰岛抗原刺激时，似乎具有更强的免疫反应性，表现为抗胰岛C'AMC增加。
