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对小鼠巨细胞病毒的遗传决定抗性:淋巴细胞抑制性巨噬细胞的作用。

Genetically determined resistance to murine cytomegalovirus: a role for lymphocytostatic macrophages.

作者信息

Price P, Winter J G, Shellam G R

机构信息

Department of Microbiology, University of Western Australia, Nedlands.

出版信息

J Gen Virol. 1987 Dec;68 ( Pt 12):2997-3008. doi: 10.1099/0022-1317-68-12-2997.

DOI:10.1099/0022-1317-68-12-2997
PMID:2826645
Abstract

Sensitivity to lethal infection with murine cytomegalovirus depends on the H-2 and background phenotype. H-2d appears to confer sensitivity in isolated cells, but sensitive BALB/c (H-2d) mice also exhibit non-specific immunosuppression which may indicate an impaired protective immune response. To determine the significance and mechanism of this immunosuppression, genetic factors controlling the activation, lymphocytostatic potential and accessory cell function of peritoneal macrophages were analysed after sub-lethal infection. In BALB/c mice, the number of peritoneal cells declined by 20% on day 3 post-infection and increased threefold over normal levels by day 7 with a progressive increase in macrophage activation and differentiation. Cells collected on day 7 exhibited lymphocytostatic activity which was not influenced by indomethacin and depressed their ability to act as accessory cells in a proliferative assay. Similar changes in the numbers of activated mature macrophages occurred in moderately resistant BALB.K (H-2k) mice showing an association with the background phenotype. In contrast peritoneal cell counts from resistant CBA (H-2k) mice were depressed by 80% on day 4 and the remaining cells enhanced the proliferation of syngeneic lymphocytes. However, later in the infection the percentage of peritoneal cells releasing virus declined rapidly and fewer cells became lymphocytostatic in both H-2k strains.

摘要

对鼠巨细胞病毒致死性感染的敏感性取决于H-2和背景表型。H-2d似乎在分离的细胞中赋予敏感性,但敏感的BALB/c(H-2d)小鼠也表现出非特异性免疫抑制,这可能表明保护性免疫反应受损。为了确定这种免疫抑制的意义和机制,在亚致死感染后分析了控制腹膜巨噬细胞激活、淋巴细胞抑制潜能和辅助细胞功能的遗传因素。在BALB/c小鼠中,感染后第3天腹膜细胞数量下降20%,到第7天比正常水平增加三倍,巨噬细胞激活和分化逐渐增加。第7天收集的细胞表现出淋巴细胞抑制活性,不受消炎痛影响,并在增殖试验中降低了它们作为辅助细胞的能力。在中等抗性的BALB.K(H-2k)小鼠中也出现了类似的活化成熟巨噬细胞数量变化,显示出与背景表型的关联。相比之下,抗性CBA(H-2k)小鼠的腹膜细胞计数在第4天下降了80%,其余细胞增强了同基因淋巴细胞的增殖。然而,在感染后期,两种H-2k品系中释放病毒的腹膜细胞百分比迅速下降,且淋巴细胞抑制作用的细胞减少。

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