Infection of human monocytes with HIV-1Ba-L. Effect on accessory cell function for T-cell proliferation in vitro.
Infection of human monocytes with HIV-1Ba-L. Effect on accessory cell function for T-cell proliferation in vitro.
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HIV-1Ba-L 感染人类单核细胞。
DOI：
10.1089/aid.1991.7.465
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发表时间：
1991
影响因子：
1.5
通讯作者：
McDougal,JS
中科院分区：
文献类型：
--
作者：
Melendez-Guerrero,LM;Nicholson,JK;McDougal,JS
人类免疫缺陷病毒(HIV)感染和获得性免疫缺陷综合征(AIDS)的主要实验室表现包括循环中的CD4+淋巴细胞水平改变和体外T细胞有丝分裂反应降低。由于T细胞的增殖是由单核细胞(Mø)调节的，因此研究确定了单核细胞功能缺陷是否是导致这些低有丝分裂反应的原因。用塑料贴壁法从正常献血者外周血单个核细胞(PBMC)中分离出摩尔。培养5d后，将贴壁细胞接种HIV-1嗜菌株BA-L。在这些条件下，在接种后5-7天就可以检测到莫尔的艾滋病毒感染。接种后10~14d，用利多卡因收集贴壁细胞，与新鲜自体T细胞和T细胞有丝分裂原共培养3d。我们发现，与未感染的单核细胞培养的T细胞相比，HIV感染的单核细胞培养的T细胞对Leu4和OKT3的增殖抗CD3反应降低，对刀豆蛋白A(ConA)的反应不同。HIV感染的Mø培养上清液可降低正常PBMC对抗CD3单抗的增殖反应。热激活的上清液也有同样的效果。HIV结合的抑制剂不能使HIV感染的培养物的增殖反应恢复到正常水平。这些结果表明，HIV感染Mø可引起可溶性因子(S)的释放，从而抑制抗CD3诱导的T细胞增殖反应。
Major laboratory manifestations of human immunodeficiency virus (HIV) infection and acquired immunodeficiency syndrome (AIDS) include altered levels of circulating CD4+lymphocytes and decreased in vitro T-cell mitogenic responses. Since T-cell proliferation is regulated by monocytes (Mø), studies were undertaken to determine whether defective Mø function contributes to these poor mitogenic responses. Mø were isolated from peripheral blood mononuclear cells (PBMC) of normal donors by adherence to plastic. After 5 days in culture, the adherent cells were inoculated with the HIV-1 Mø-tropic strain, Ba-L. Under these conditions HIV infection in Mø can be detected 5-7 days after inoculation. Ten to fourteen days postinoculation, the adherent cells were harvested with lidocaine and cocultured with fresh autologous T cells and T-cell mitogens in a 3-day assay. We found decreased proliferative anti-CD3 responses to Leu4 and OKT3 and variable responses to concanavalin A (Con A) by T cells cultured with HIV-infected monocytes compared with T cells cultured with uninfected Mø. Supernatants from HIV-infected Mø cultures decreased proliferative responses of normal PBMC to anti-CD3 monoclonal antibodies. Heat-activated supernatants had the same effect. Inhibitors of HIV binding did not restore proliferative responses of HIV-infected cultures to normal levels. These results indicate that HIV infection of Mø causes the release of soluble factor(s) that suppress anti-CD3-induced T-cell proliferative responses.