Rose A H, Holt P G, Turner K J
Int Arch Allergy Appl Immunol. 1982;67(4):356-61. doi: 10.1159/000233047.
The activity of resident and exudate peritoneal macrophages from mice maintained on a low protein diet (4% casein initiated at weaning) was assessed in a variety of assay systems which examined aspects of macrophage 'immunogenic' function in vivo and in vitro. Antigen-pulsed macrophages from malnourished mice triggered secondary IgE and IgG responses following intraperitoneal inoculation into pre-immunized syngeneic recipients. Similarly, intraperitoneal transfer of low numbers of these cells successfully primed immunologically naive syngeneic mice; in both cases, the activity of macrophages from malnourished mice could not be distinguished from these derived from normal animals. Examination of uptake and breakdown of radio-labelled antigen revealed normal rates of phagocytosis, and a brief lag in the early phase of degradation, relative to control macrophages. Antigen-pulsed macrophages from malnourished mice were severely impaired in their capacity to trigger the proliferation of antigen-primed T cells in vitro.
在各种检测系统中评估了以低蛋白饮食(断奶时开始给予4%酪蛋白)饲养的小鼠的腹腔常驻巨噬细胞和渗出巨噬细胞的活性,这些检测系统检测了巨噬细胞在体内和体外的“免疫原性”功能方面。营养不良小鼠的抗原脉冲巨噬细胞在腹腔接种到预先免疫的同基因受体后引发了继发性IgE和IgG反应。同样,少量这些细胞的腹腔转移成功地启动了免疫未成熟的同基因小鼠;在这两种情况下,营养不良小鼠的巨噬细胞活性与正常动物来源的巨噬细胞活性没有区别。对放射性标记抗原的摄取和分解的检查显示吞噬率正常,相对于对照巨噬细胞,降解早期有短暂延迟。营养不良小鼠的抗原脉冲巨噬细胞在体外触发抗原致敏T细胞增殖的能力严重受损。