Sai P, Boitard C, Debray-Sachs M, Pouplard A, Assan R, Hamburger J
Diabetes. 1981 Dec;30(12):1051-7. doi: 10.2337/diab.30.12.1051.
To explore humoral immunity in insulin-dependent diabetic (IDDM) patients, we studied insulin release from isolated mouse islets stimulated by glucose + theophylline after incubation with the sera of these patients and complement. Eleven of 21 IDDM sera suppressed the stimulated insulin release while the arginine-stimulated glucagon release remained unchanged. Morphologic evidence and the trypan-blue exclusion test suggested that the suppression of insulin release was due to a cytotoxic effect of the sera. No beta-cell inhibition of morphologic damage was detectable in the presence of sera from 30 healthy subjects, 8 non-insulin-dependent diabetic patients, and 5 nondiabetic patients with autoimmune diseases. Beta-cell inhibition by IDDM sera was not observed when complement was omitted. After serum fractionation, the cytotoxic potency of IDDM sera was located in the immunoglobulin G fraction. Using human islets, insulin release was suppressed by 3 of 6 IDDM sera. Complement-dependent cytotoxicity was found in 1 of 5 recent-onset IDDM patients and 11 of 16 IDDM patients with autoimmune phenomena. It was associated in all cases with the presence of islet cell antibodies as detected by immunofluorescence, and with the presence of circulating lymphocytes which suppressed insulin release in vitro. Complement-fixing antibodies may contribute to the selective beta-cell damage in IDDM.
为了探究胰岛素依赖型糖尿病（IDDM）患者的体液免疫，我们研究了在将这些患者的血清与补体孵育后，葡萄糖 + 茶碱刺激下分离的小鼠胰岛的胰岛素释放情况。21份IDDM血清中有11份抑制了刺激后的胰岛素释放，而精氨酸刺激的胰高血糖素释放则保持不变。形态学证据和台盼蓝排斥试验表明，胰岛素释放的抑制是由于血清的细胞毒性作用。在30名健康受试者、8名非胰岛素依赖型糖尿病患者和5名患有自身免疫性疾病的非糖尿病患者的血清存在的情况下，未检测到对形态学损伤的β细胞抑制作用。当省略补体时，未观察到IDDM血清对β细胞的抑制作用。血清分级分离后，IDDM血清的细胞毒性效力位于免疫球蛋白G组分中。使用人胰岛，6份IDDM血清中有3份抑制了胰岛素释放。在5名近期发病的IDDM患者中有1名以及16名有自身免疫现象的IDDM患者中有11名发现了补体依赖性细胞毒性。在所有病例中，它都与免疫荧光检测到的胰岛细胞抗体的存在以及体外抑制胰岛素释放的循环淋巴细胞的存在有关。补体结合抗体可能导致IDDM中选择性β细胞损伤。
