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首页> 外文期刊>Journal of Virology >Influenza virus-induced immune complexes suppress alveolar macrophage phagocytosis.
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Influenza virus-induced immune complexes suppress alveolar macrophage phagocytosis.

机译：流感病毒诱导的免疫复合物抑制肺泡巨噬细胞吞噬作用。

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Immune complexes in the lungs are capable of inducing adverse responses. Herein we have detailed the formation of immune complexes in the lungs of influenza virus-infected mice and examined their effect on alveolar macrophage defenses. On days 3, 7, 10, 15, and 30 after aerosol infection with influenza A/PR8/34 virus, the acellular pulmonary lavage fluid was tested for viral antigen, specific viral antibody, and immune complexes by immunoassays. Whereas peak viral antigen (day 3) diminished to undetectable levels by day 10, specific viral antibody remained at a low concentration until day 10, after which it rapidly increased. Immune complex concentrations increased through day 7, peaked at day 10, and gradually returned to the control level by day 30. These data demonstrate that immune complexes of detectable size are induced by influenza virus infection during the interface between antigen excess and antibody excess conditions. Since alveolar macrophages are the pivotal phagocytic defense cells in the lung, the ability of normal alveolar macrophages to ingest opsonized erythrocytes was quantitated in the presence of immune complexes from lavage fluid. Immune complexes from day 10 virus-infected lungs caused a dose-dependent suppression of antibody-mediated phagocytosis to 30% of control values. In contrast, although these immune complexes also markedly decreased the phagocytosis of antibody-coated yeast cells, they did not significantly impair the antibody-independent ingestion of unopsonized yeast cells by macrophages. the suppressive effects of immune complexes on alveolar macrophages may, in part, explain the phagocytic dysfunction that occurs 7 to 10 days after influenza virus pneumonia.
机译：肺中的免疫复合物能够诱导不良反应。在此，我们详细介绍了流感病毒感染的小鼠的肺部免疫复合物的形成，并检查了对肺泡巨噬细胞防御的影响。在气溶胶感染气溶胶感染后的第3,7,10,15和30天，通过免疫测定对病毒抗原，特异性病毒抗体和免疫复合物进行缩细胞肺灌洗液。然而，峰值病毒抗原（第3天）在第10天减少到未检测到的水平，但特异性病毒抗体保持低浓度至第10天，之后迅速增加。免疫复合物浓度通过第7天增加，在第10天达到峰值，并逐渐返回到第30天的控制水平。这些数据表明，可检测大小的免疫复合物在抗原过量和抗体过量条件之间的界面之间被流感病毒感染诱导。由于肺泡巨噬细胞是肺部中的枢轴吞噬细胞，因此在免疫复合物存在下，定量正常肺泡巨噬细胞对来自灌洗液的免疫复合物存在的能力。来自第10天病毒感染肺的免疫复合物导致抗体介导的吞噬作用的剂量依赖性抑制至30％的对照值。相反，虽然这些免疫复合物也显着降低了抗体涂覆的酵母细胞的吞噬作用，但它们并未显着损害通过巨噬细胞对非团体酵母细胞的抗体独立摄取。免疫复合物对肺泡巨噬细胞的抑制作用可以部分地解释流感病毒肺炎后7至10天发生的吞噬功能障碍。

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