Köhler E, Knospe S, Besch W, Michaelis D, Rjasanowski I
Central Institute of Diabetes Gerhardt Katsch, Karlsburg, GDR.
Exp Clin Endocrinol. 1989;94(3):357-62. doi: 10.1055/s-0029-1210922.
ADCC (antibody-dependent cellular cytotoxicity) against xenogenic islets in vitro has frequently been found with mononuclear blood cells and heat inactivated autologous serum from newly diagnosed Type-1 diabetics. Anti-islet ADCC, as measured by enhanced 51Cr-release of islets after a 6h-incubation, leads to functional alteration of islets such as a decrease in insulin content and in leucine incorporation. In a follow-up investigation over at least three years it was demonstrated that anti-islet ADCC in vitro disappears, if there is no more C-peptide secretion in vivo. Furthermore, anti-islet ADCC has also not been found in long-term Type-1 diabetics who had no C-peptide secretion but an acutely stimulated immune system due to infectious diseases. An acute immunocytolytic process against pancreatic beta cells in vivo seems to be the precondition for anti-islet ADCC in vitro.
在体外，经常发现来自新诊断的1型糖尿病患者的单核血细胞和热灭活自体血清对异种胰岛具有抗体依赖性细胞毒性（ADCC）。通过6小时孵育后胰岛51Cr释放增强来测量的抗胰岛ADCC会导致胰岛功能改变，如胰岛素含量和亮氨酸掺入量减少。在至少三年的后续研究中表明，如果体内不再有C肽分泌，体外抗胰岛ADCC就会消失。此外，在没有C肽分泌但因传染病而免疫系统受到急性刺激的长期1型糖尿病患者中也未发现抗胰岛ADCC。体内针对胰腺β细胞的急性免疫溶解过程似乎是体外抗胰岛ADCC的前提条件。
