Leu R W, Rummage J A, Horn M J
Biomedical Division, Samuel Roberts Noble Foundation, Inc., Ardmore, Oklahoma.
Immunobiology. 1989 Feb;178(4-5):340-50. doi: 10.1016/S0171-2985(89)80057-9.
Resident and oil-elicited inflammatory peritoneal macrophages (PM phi) from competent C3HeB/FeJ and genetically deficient C3H/HeJ mice were characterized for their Fc receptor (FcR)-dependent binding, phagocytic and ADCC functions during in vitro differentiation under the influence of mouse recombinant interferon-gamma (rIFN-gamma), interferon-alpha/beta (IFN-alpha/beta) fetal bovine serum (FBS), or in serum-free medium. Freshly cultured resident PM phi from C3HeB/FeJ mice had low levels of FcR-mediated phagocytosis in response to mouse monoclonal IgG gamma 2a, IgG gamma 2b or IgG gamma 1, opsonized sheep erythrocytes as compared to oil-elicited inflammatory PM phi from the same strain. Resident PM phi were uniformly upregulated in their FcR-dependent phagocytosis after 24-48 h in vitro culture with FBS to levels approximating that of freshly cultured inflammatory PM phi which were also further upregulated after 24 h in vitro culture with FBS. Both resident and inflammatory PM phi were upregulated largely by an autostimulatory process in that they increased their FcR-mediated phagocytosis in serum-free RPMI-1640 medium without the addition of rIFN-gamma or IFN-alpha/beta, although FBS further augmented FcR upregulation. A synergistic effect of FBS and rIFN-gamma was required for total reconstitution of FcR-mediated phagocytosis of FcR-incompetent C3H/HeJ inflammatory PM phi in that FBS or rIFN-gamma alone only partially reconstituted FcR function, whereas in combination full reconstitution occurred. Thus, macrophages from competent C3HeB/FeJ mice were upregulated in their FcR-mediated functions largely by an autostimulatory process, presumably dependent on endogenous of IFN-beta, whereas, genetically-deficient C3H/HeJ macrophages required exogenous rIFN-gamma in combination with fetal bovine serum for synergistic reconstitution of FcR functions. The uniform upregulation of FcR-dependent effector functions in vitro appears to provide an efficient system for enhanced immune function during differentiation which may be applicable to in vivo situations.
在小鼠重组干扰素 -γ（rIFN -γ）、干扰素 -α/β（IFN -α/β）、胎牛血清（FBS）的影响下，或在无血清培养基中，对来自具有补体活性的C3HeB/FeJ小鼠和基因缺陷的C3H/HeJ小鼠的驻留型和油诱导的炎性腹腔巨噬细胞（PM phi）的Fc受体（FcR）依赖性结合、吞噬和ADCC功能进行了体外分化过程中的特性研究。与来自同一品系的油诱导炎性PM phi相比，来自C3HeB/FeJ小鼠的新鲜培养的驻留型PM phi对小鼠单克隆IgGγ2a、IgGγ2b或IgGγ1调理的绵羊红细胞的FcR介导的吞噬作用水平较低。驻留型PM phi在与FBS进行24 - 48小时体外培养后，其FcR依赖性吞噬作用均匀上调至接近新鲜培养的炎性PM phi的水平，而新鲜培养的炎性PM phi在与FBS进行24小时体外培养后也进一步上调。驻留型和炎性PM phi在很大程度上通过自刺激过程上调，因为它们在无血清的RPMI - 1640培养基中增加了FcR介导的吞噬作用，而无需添加rIFN -γ或IFN -α/β，尽管FBS进一步增强了FcR上调。FBS和rIFN -γ的协同作用是FcR功能不全的C3H/HeJ炎性PM phi的FcR介导吞噬作用完全重建所必需的，因为单独的FBS或rIFN -γ仅部分重建FcR功能，而联合使用则发生完全重建。因此，来自具有补体活性的C3HeB/FeJ小鼠的巨噬细胞在很大程度上通过自刺激过程上调其FcR介导的功能，推测依赖于内源性IFN -β，而基因缺陷的C3H/HeJ巨噬细胞需要外源性rIFN -γ与胎牛血清协同重建FcR功能。体外FcR依赖性效应功能的均匀上调似乎为分化过程中增强免疫功能提供了一个有效的系统，这可能适用于体内情况。
