Hanahoe T H
Agents Actions. 1984 Apr;14(3-4):468-74. doi: 10.1007/BF01973851.
In vivo passive sensitization of rat peritoneal mast cells with Nippostrongylus braziliensis antiserum or rat monoclonal myeloma IgE greatly enhanced histamine release in vitro by dextran or anti IgE, but did not alter release by compound 48/80 or A23187. Conversely, removal of IgE from the cells by acid pH abolished histamine release by dextran and anti IgE but did not impair release by compound 48/80. Whereas, histamine release from cells isolated from rats genetically resistant to dextran (NR rats) by anti IgE was potentiated by passive sensitization, dextran was unable to stimulate secretion from control or sensitized NR cells. The results suggest that dextran releases histamine by interaction with cell-fixed IgE and that the NR mast cell membrane lacks the ability to interpret this stimulus.
用巴西日圆线虫抗血清或大鼠单克隆骨髓瘤IgE对大鼠腹腔肥大细胞进行体内被动致敏,可大大增强体外由葡聚糖或抗IgE诱导的组胺释放,但不改变由化合物48/80或A23187诱导的释放。相反,通过酸性pH从细胞中去除IgE可消除葡聚糖和抗IgE诱导的组胺释放,但不损害化合物48/80诱导的释放。然而,抗IgE可增强从对葡聚糖遗传抗性大鼠(NR大鼠)分离的细胞中组胺的释放,而葡聚糖不能刺激对照或致敏NR细胞的分泌。结果表明,葡聚糖通过与细胞固定的IgE相互作用释放组胺,并且NR肥大细胞膜缺乏解读这种刺激的能力。