Wassef N M, Roerdink F, Richardson E C, Alving C R
Proc Natl Acad Sci U S A. 1984 May;81(9):2655-9. doi: 10.1073/pnas.81.9.2655.
Increased phagocytosis of complement-opsonized vesicles was accompanied by increased phosphatidylinositol (PtdIns) turnover in murine macrophages. However when PtdIns was also present as one of the lipids in the opsonized liposomes, it reduced both phagocytosis and stimulation of endogenous PtdIns turnover. These suppressive effects did not occur with liposomes containing PtdIns phosphate (PtdIns-P). When a monoclonal IgM "anti-PtdIns-P" antibody that bound to inositol phosphate was substituted for antigalactosyl ceramide antibodies for activating complement in the opsonizing process, enhanced phagocytosis occurred normally but increased cellular PtdIns turnover did not occur. Therefore the data show that, although PtdIns-P cannot replace PtdIns for suppressing PtdIns turnover, PtdIns-P can be induced to be suppressive after specific binding to an antibody that recognizes inositol phosphate. We conclude that ingestion of complement-opsonized liposomes by macrophages and complement-induced turnover of cellular PtdIns are separate but related phenomena that can be independently modulated by the polar group of liposomal PtdIns.
在小鼠巨噬细胞中，补体调理的囊泡吞噬作用增强伴随着磷脂酰肌醇（PtdIns）周转率的增加。然而，当PtdIns也作为调理脂质体中的一种脂质存在时，它会降低吞噬作用和内源性PtdIns周转率的刺激。含磷酸磷脂酰肌醇（PtdIns-P）的脂质体不会产生这些抑制作用。当一种与磷酸肌醇结合的单克隆IgM“抗PtdIns-P”抗体在调理过程中替代抗半乳糖基神经酰胺抗体来激活补体时，吞噬作用正常增强，但细胞PtdIns周转率没有增加。因此，数据表明，虽然PtdIns-P不能替代PtdIns来抑制PtdIns周转率，但PtdIns-P在与识别磷酸肌醇的抗体特异性结合后可被诱导产生抑制作用。我们得出结论，巨噬细胞摄取补体调理的脂质体和补体诱导的细胞PtdIns周转率是相互独立但又相关的现象，它们可由脂质体PtdIns的极性基团独立调节。
