Griffin F M, Mullinax P J
J Immunol. 1985 Jul;135(1):344-9.
We previously described a unique lymphokine that activates macrophage C3 receptors for phagocytosis. The lymphokine is generated when T lymphocytes receive a signal from macrophages that have ingested IgG-coated material. In the present work, we examined the mechanisms by which macrophage Fc receptors must be engaged for macrophages to signal lymphocytes to elaborate the lymphokine. We found that ingestion mediated by any of the three classes of murine macrophage Fc receptors was sufficient to trigger macrophages, and that engagement of macrophage Fc receptors by immobilized immune complexes was effective as well. We also found that ligation of Fc receptors by an anti-Fc receptor IgG antibody or by its F(ab')2 or Fab fragments also triggered macrophages. The ability of monovalent ligation of the receptor to elicit biologic activity suggests that this system may be of value in elucidating general mechanisms by which ligand binding of receptors is transduced into biologic effects.
我们之前描述了一种独特的淋巴因子,它可激活巨噬细胞的C3受体以促进吞噬作用。当T淋巴细胞接收到来自已摄取IgG包被物质的巨噬细胞发出的信号时,就会产生这种淋巴因子。在目前的研究中,我们研究了巨噬细胞的Fc受体必须被激活才能向淋巴细胞发出信号以产生淋巴因子的机制。我们发现,由三类小鼠巨噬细胞Fc受体中的任何一种介导的摄取足以触发巨噬细胞,并且固定化免疫复合物与巨噬细胞Fc受体的结合也有效。我们还发现,抗Fc受体IgG抗体或其F(ab')2或Fab片段与Fc受体的连接也能触发巨噬细胞。受体的单价连接引发生物学活性的能力表明,该系统可能有助于阐明受体的配体结合如何转化为生物学效应的一般机制。