Kolb H, Freytag G, Kiesel U, Kolb-Bachofen V
Clin Exp Immunol. 1981 Jan;43(1):121-7.
We studied autoimmune reactions against pancreatic islets occurring as a consequence of defects of the immune system rather than after pathological changes in the endocrine organ itself. Immune dysregulation was induced by transfer of parental lymphocytes into semi-allogeneic F1 recipient mice (graft versus host reaction, GVHR). Recipients were killed 1 month after the induction of the disease. Pancreatic islets were screened by light microscopy for signs of lymphocytic infiltration (insulitis). Severe insulitis was found in all mice undergoing GVHR. The cytotoxic activity of lymphocytes was apparent in electron microscopic studies and affected only B cells. Infiltrations were not seen in the exocrine part of the pancreas nor in heart, liver or kidneys at this early stage of GVHR. It is concluded that non-specific disorders of the immune system induced by GVHR may lead to specific cellular autoimmune reactions against B cells of pancreatic islets.
我们研究了免疫系统缺陷导致的针对胰岛的自身免疫反应，而非内分泌器官自身发生病理变化之后出现的此类反应。通过将亲代淋巴细胞转移至半同种异体F1受体小鼠体内（移植物抗宿主反应，GVHR）来诱导免疫失调。在疾病诱导1个月后处死受体小鼠。通过光学显微镜检查胰岛，寻找淋巴细胞浸润（胰岛炎）迹象。在所有经历GVHR的小鼠中均发现了严重的胰岛炎。淋巴细胞的细胞毒性活性在电子显微镜研究中很明显，且仅影响B细胞。在GVHR的这个早期阶段，胰腺外分泌部分以及心脏、肝脏或肾脏中均未观察到浸润现象。得出的结论是，GVHR诱导的免疫系统非特异性紊乱可能导致针对胰岛B细胞的特异性细胞自身免疫反应。
