Fukushima K, Takasaki S
Department of Biochemistry, University of Tokyo, Japan.
Biochem Biophys Res Commun. 1993 Apr 30;192(2):333-7. doi: 10.1006/bbrc.1993.1419.
By culturing with tunicamycin A1, an inhibitor of N-glycosylation, or by sialidase digestion, mouse monocytic cells P388D1 were induced to carry out Fc receptor-mediated phagocytosis of IgG-coated sheep red blood cells. There was no significant difference in the numbers of IgG-coated sheep blood cells bound to the cells at 4 degrees C before and after exposure to tunicamycin or sialidase. These results suggest that sialylated N-glycans expressed on the cell surface have a suppressive role in the induction of phagocytosis, and their decreased expression or reduced sialylation results in acquisition of the phagocytic ability of the cells by affecting some processes involved in the ingestion of the particles bound to Fc receptors.
通过用N-糖基化抑制剂衣霉素A1培养,或通过唾液酸酶消化,诱导小鼠单核细胞P388D1进行IgG包被的绵羊红细胞的Fc受体介导的吞噬作用。在4℃下,暴露于衣霉素或唾液酸酶前后,与细胞结合的IgG包被的绵羊血细胞数量没有显著差异。这些结果表明,细胞表面表达的唾液酸化N-聚糖在吞噬作用的诱导中具有抑制作用,其表达降低或唾液酸化减少会通过影响与Fc受体结合颗粒摄取相关的一些过程,导致细胞获得吞噬能力。