Lee S H, Crocker P, Gordon S
J Exp Med. 1986 Jan 1;163(1):54-74. doi: 10.1084/jem.163.1.54.
We have studied the effect of infection with the blood-stage of Plasmodium yoelii 17X, a nonlethal parasite, on plasma membrane antigens, receptors, and secretory properties of macrophages (M phi) in murine liver, spleen, and blood. mAb F4/80 (M phi specific), F7/4 (a marker for immature and immunologically activated M phi, as well as neutrophils), and Mac-1, which binds to the type 3 complement receptor, were used to measure the distribution and total content of antigens in situ and to assay surface expression of antigens on M phi isolated by collagenase perfusion-digestion and adherence. We also examined respiratory burst activity after stimulation with PMA, FcR activity, Ia antigen expression, and binding of 125I-mannose-BSA and unopsonized sheep erythrocytes by isolated M phi. In the normal animal, spleen M phi expressed Mac-1 and F7/4 antigens and relatively high levels of respiratory burst activity, in contrast to Kupffer cells in liver, where all three features were virtually absent. The introduction of parasitized erythrocytes into the circulation resulted in a large influx of F4/80+ M phi into the blood, liver, and spleen, where local M phi proliferation could also contribute. Liver M phi during malaria infection showed increased Mac-1 and 7/4 antigen and an increased respiratory burst potential compared with uninfected controls. Increases in total, but not specific activity of FcR, Ia antigen, and binding of unopsonized sheep erythrocytes were found in spleen and liver M phi populations after infection. In both populations, there was an early but persistent marked reduction in specific binding and uptake of 125I-mannose-BSA. These results confirm and extend observations that normal Kupffer cells are relatively homogeneous in morphology, surface markers, and anatomical location, in contrast to M phi in normal spleen, and that both of these populations differ from resident M phi elsewhere, including the peritoneal cavity. In the course of infection by P. yoelii, M phi with high levels of opsonic receptors (CR3, FcR) and respiratory burst potential are mobilized in large numbers at specific sites such as liver and spleen, in accordance with an important role for M phi in the clearance of parasitized erythrocytes from blood.
我们研究了感染约氏疟原虫17X(一种非致死性寄生虫)血液阶段对小鼠肝脏、脾脏和血液中巨噬细胞(M phi)的质膜抗原、受体及分泌特性的影响。使用单克隆抗体F4/80(M phi特异性)、F7/4(未成熟及免疫激活的M phi以及中性粒细胞的标志物)和与3型补体受体结合的Mac-1来原位测量抗原的分布和总量,并检测经胶原酶灌注消化及贴壁分离的M phi上抗原的表面表达。我们还检测了经佛波酯(PMA)刺激后的呼吸爆发活性、FcR活性、Ia抗原表达以及分离的M phi对125I-甘露糖-BSA和未调理的绵羊红细胞的结合情况。在正常动物中,脾脏M phi表达Mac-1和F7/4抗原,且呼吸爆发活性水平相对较高,而肝脏中的库普弗细胞则几乎不具备这三个特征。将感染疟原虫的红细胞引入循环会导致大量F4/80+ M phi涌入血液、肝脏和脾脏,局部M phi增殖也可能起作用。与未感染的对照组相比,疟疾感染期间肝脏M phi的Mac-1和7/4抗原增加,呼吸爆发潜能增强。感染后在脾脏和肝脏M phi群体中发现FcR、Ia抗原总量增加,但特异性活性未增加,未调理的绵羊红细胞结合增加。在这两个群体中,125I-甘露糖-BSA的特异性结合和摄取均早期出现且持续显著降低。这些结果证实并扩展了以下观察结果:正常库普弗细胞在形态、表面标志物和解剖位置上相对均一,与正常脾脏中的M phi不同,且这两个群体均与包括腹腔在内的其他部位的驻留M phi不同。在约氏疟原虫感染过程中,具有高水平调理受体(CR3、FcR)和呼吸爆发潜能的M phi会在肝脏和脾脏等特定部位大量动员,这与M phi在清除血液中感染疟原虫的红细胞方面的重要作用相一致。