Macrophage plasma membrane and secretory properties in murine malaria. Effects of Plasmodium yoelii blood-stage infection on macrophages in liver, spleen, and blood.
Macrophage plasma membrane and secretory properties in murine malaria. Effects of Plasmodium yoelii blood-stage infection on macrophages in liver, spleen, and blood.
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DOI：
10.1084/jem.163.1.54
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发表时间：
1986-01-01
期刊：
影响因子：
--
通讯作者：
Gordon S
中科院分区：
文献类型：
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作者：
Lee SH;Crocker P;Gordon S
我们研究了感染血液阶段的约氏疟原虫17X，一种非致命的寄生虫，对质膜抗原，受体和分泌特性的巨噬细胞（M phi）在小鼠肝脏，脾脏和血液的影响。mAb F4/80（M phi特异性）、F7/4（未成熟和免疫活化M phi以及中性粒细胞的标志物）和Mac-1（与3型补体受体结合）用于原位测量抗原的分布和总含量，并测定通过胶原酶灌注消化和粘附分离的M phi上抗原的表面表达。我们还研究了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与125 I-甘露糖-BSA和未调理的绵羊红细胞的结合。在正常动物中，脾脏M phi表达Mac-1和F7/4抗原和相对高水平的呼吸爆发活性，与肝脏中的枯否细胞相反，肝脏中的所有三个特征几乎都不存在。将寄生的红细胞引入循环导致大量F4/80 + M phi流入血液、肝脏和脾脏，其中局部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M phi显示Mac-1和7/4抗原增加，呼吸爆发潜力增加。感染后，在脾脏和肝脏M phi人群中发现FcR，Ia抗原和未调理绵羊红细胞结合的总活性增加，但特异性活性没有增加。在这两个群体中，有一个早期的，但持续的显着减少特异性结合和摄取的125I-甘露糖-BSA。这些结果证实并扩展了正常枯否细胞在形态、表面标记和解剖位置上相对均一的观察结果，与正常脾脏中的M phi相反，并且这两个群体与其他地方的居民M phi不同，包括腹膜腔。在约氏疟原虫感染过程中，具有高水平调理素受体（CR3、FcR）和呼吸爆发电位的M phi在特定部位（如肝和脾）大量动员，这与M phi在从血液中清除寄生红细胞中的重要作用一致。
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.