Appels B, Burkart V, Kantwerk-Funke G, Funda J, Kolb-Bachofen V, Kolb H
Diabetes Research Institute, University of Düsseldorf, FRG.
J Immunol. 1989 Jun 1;142(11):3803-8.
Activated peritoneal macrophages were found to lyse syngeneic [3H]leucine-labeled pancreatic islet cells or rat insulinoma cells after 15 h of coculture at 37 degrees C. Lysis was verified by electron microscopic analysis. Islet cell lysis was dependent on the T:E ratio and was comparable with P815 and L929 tumor cells used as targets. The cytotoxic activity was localized in the adherent fraction of Corynebacterium parvum activated peritoneal cells and was destroyed by incubation of cells with macrophage-toxic silica particles. Syngeneic thyrocytes and hepatocytes were found to be resistant to the cytolytic action of activated macrophages. It has been shown previously that macrophages contribute to pancreatic islet inflammation. The present in vitro analysis demonstrates that macrophages can function as effector cells in islet destruction.
在37℃共培养15小时后,发现活化的腹膜巨噬细胞可裂解同基因的[3H]亮氨酸标记的胰岛细胞或大鼠胰岛素瘤细胞。通过电子显微镜分析证实了细胞裂解。胰岛细胞裂解取决于T:E比例,并且与用作靶标的P815和L929肿瘤细胞相当。细胞毒性活性定位于短小棒状杆菌活化的腹膜细胞的贴壁部分,并且通过用巨噬细胞毒性二氧化硅颗粒孵育细胞而被破坏。发现同基因的甲状腺细胞和肝细胞对活化巨噬细胞的溶细胞作用具有抗性。先前已经表明巨噬细胞促成胰岛炎症。目前的体外分析表明巨噬细胞可以作为胰岛破坏中的效应细胞发挥作用。