A low molecular weight phagocytosis-inhibitory factor obtained from human erythrocyte membranes specifically down-regulates Mac-1 activity on tetradecanoyl phorbol acetate-stimulated monocytic cell lines in a Ca(2+)-dependent manner.
A low molecular weight phagocytosis-inhibitory factor obtained from human erythrocyte membranes specifically down-regulates Mac-1 activity on tetradecanoyl phorbol acetate-stimulated monocytic cell lines in a Ca(2+)-dependent manner.
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从人红细胞膜获得的低分子量吞噬抑制因子以 Ca(2) 依赖性方式特异性下调十四酰佛波醇乙酸酯刺激的单核细胞系上的 Mac-1 活性。
作者：
K. Baranji;L. Baranyi;T. Yoshida;N. Okada;H. Okada
从人红细胞膜中部分纯化了一种低分子量（< 3 kDa）的吞噬抑制因子（PIF）。PIF以Ca（2+）依赖性方式抑制巨噬细胞样细胞的乳胶吞噬作用和C以及FcR介导的吞噬作用。这种吞噬抑制活性是可逆的，因为去除PIF恢复了细胞的吞噬能力。在用PIF处理后，通过使用mAb D-12和BEAR-1的免疫荧光染色，Mac-1 Ag（CR 3或CD 11b）在细胞表面上变得几乎检测不到，而用LM 2/1抗Mac-1 mAb染色证明Mac-1仍然存在于细胞表面上，因此表明Mac-1可能发生构象变化。PIF对CR 1（CD 35）、CR2（CD 21）、20-kDa同源限制因子（CD 59）、衰变加速因子（CD 55）、LFA-1（CD 11 a）或p150.95（CD 11 c）的染色无显著抑制作用。尽管携带Mac-1的U-937细胞与经C3双调理的珠粒的结合被完全阻断，但通过Con A和FcR的结合仍然不受PIF处理的影响。除了对吞噬作用的抑制作用外，还观察到对细胞粘附的抑制。PIF对细胞粘附的抑制作用不是单核细胞特异性的，因为在暴露于PIF后，TGW神经母细胞瘤细胞系失去了其附着于组织培养板的能力，但保留了其同型聚集的能力。PIF是一种天然的红细胞吞噬调节剂的可能性建议。
A low molecular mass (< 3 kDa) phagocytosis-inhibitory factor (PIF), was partially purified from human erythrocyte membranes. PIF inhibits latex phagocytosis and C, as well as FcR-mediated phagocytosis, by macrophage-like cells in a Ca(2+)-dependent manner. This phagocytosis-inhibitory activity is reversible because removal of PIF restores phagocytic capability of cells. After treatment with PIF, Mac-1 Ag (CR3 or CD11b) becomes almost undetectable on the cell surface by immunofluorescence staining using the mAbs D-12 and BEAR-1, whereas staining with the LM2/1 anti-Mac-1 mAb proved that Mac-1 is still present on the cell surface, thus, indicating a possible conformational change in Mac-1. PIF has no significant inhibitory effect on staining of CR1 (CD35), CR2, (CD21), 20-kDa homologous restriction factor (CD59), decay-accelerating factor (CD55), LFA-1 (CD11a), or p150.95 (CD11c). Although binding of Mac-1-bearing U-937 cells to C3bi-opsonized beads is completely blocked, binding via Con A and FcRs remains unaffected by PIF treatment. In addition to the suppressive effect on phagocytosis, inhibition of cell adhesion was observed as well. The inhibitory effect of PIF on cell adhesion is not monocyte specific, because after exposure to PIF the TGW neuroblastoma cell line lost its ability to attach to the tissue culture plate, but retained its ability for homotypic aggregation. The possibility that PIF is a natural regulator of erythrophagocytosis is suggested.