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首页> 外文期刊>Infection and immunity >Influence of Malaria Infection on the Elaboration of Soluble Mediators by Adherent Mononuclear Cells
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Influence of Malaria Infection on the Elaboration of Soluble Mediators by Adherent Mononuclear Cells

机译：疟疾感染对粘附性单核细胞精制可溶性介体的影响

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Malaria results in two seemingly paradoxical perturbations of the immune response: polyclonal B-cell activation and immunosuppression. To determine what immunoregulatory role mediators secreted by adherent cells might play in these alterations, we cultured adherent cells from uninfected mice and from mice at different times during infection with Plasmodium berghei or P. yoelii. Culture supernatants obtained from these cells were tested for their ability to enhance the in vitro proliferative responses of thymocytes to suboptimal concentrations of concanavalin A or to inhibit the mitogen-stimulated proliferation of normal spleen cells. Supernatants obtained from adherent cells of mice early in infection (days 1 to 3) contained significantly elevated levels of enhancing activity which on Bio-Gel P-100 chromatography resembled lymphocyte-activating factor. Later in infection (days 4 and 5), these supernatants contained inhibitory activity. Normal adherent cells, when cocultivated in vitro with parasitized erythrocytes, ingested parasite debris and were stimulated to produce the enhancing factor. At high parasite/adherent-cell ratios, cells elaborated an inhibitory factor. These findings suggest that during malaria, adherent cells are converted from a nonspecific helper role to a nonspecific suppressor role. This modulation in function may be due to the direct interaction between adherent cells and parasitized erythrocytes.
机译：疟疾导致免疫应答出现两个看似矛盾的干扰：多克隆B细胞活化和免疫抑制。为了确定贴壁细胞分泌的免疫调节剂在这些改变中可能发挥的作用，我们培养了未感染小鼠和在感染伯氏疟原虫或 P的不同时间来自小鼠的贴壁细胞。测试从这些细胞获得的培养上清液增强胸腺细胞对次最佳浓度的伴刀豆球蛋白A的体外增殖反应或抑制有丝分裂原刺激的正常脾细胞增殖的能力。从感染早期（第1至3天）的小鼠贴壁细胞中获得的上清液，其增强活性水平显着升高，在Bio-Gel P-100色谱上类似于淋巴细胞活化因子。在感染后期（第4天和第5天），这些上清液具有抑制活性。正常的贴壁细胞在体外与被寄生的红细胞共培养时，会摄入寄生虫碎片并被刺激产生增强因子。在高的寄生虫/贴壁细胞比例下，细胞形成了抑制因子。这些发现表明在疟疾期间，贴壁细胞从非特异性的辅助作用转变为非特异性的抑制作用。功能上的这种调节可能是由于贴壁细胞和被寄生的红细胞之间的直接相互作用。

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