Interleukin-12 decreases human immunodeficiency virus type 1 replication in human macrophage cultures reconstituted with autologous peripheral blood mononuclear cells.
Interleukin-12 decreases human immunodeficiency virus type 1 replication in human macrophage cultures reconstituted with autologous peripheral blood mononuclear cells.
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Interleukin-12 可减少用自体外周血单核细胞重建的人巨噬细胞培养物中人类免疫缺陷病毒 1 型的复制。
DOI：
10.1093/infdis/173.3.559
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Reed,SG
中科院分区：
文献类型：
--
作者：
Akridge,RE;Reed,SG
研究了白细胞介素(IL)-12、干扰素(IFN)-γ和人类免疫缺陷病毒（HIV） 1型感染在人巨噬细胞中的体外相互作用。巨噬细胞被hiv - 1感染，并与自体单核细胞缺失的外周血单核细胞（PBMC）共培养。在hiv -1感染的巨噬细胞中加入自体PBMC可导致逆转录酶（RT）活性的大幅增加；然而，当加入自体PBMC和IL-12时，RT活性降低（75%-90%），并检测到高水平的IFN-γ (9-16 ng/mL)。抗ifn -γ抗体的加入阻断了il -12诱导的RT活性下降。令人惊讶的是，将外源性IL-12添加到没有自体淋巴细胞的hiv感染巨噬细胞培养物中导致RT活性降低50%-60%，而IFN-γ未检测到增加。抗ifn -γ的加入并没有抑制这种il -12介导的作用。这些结果表明，IL-12能够间接下调用自体PBMC重组巨噬细胞培养的HIV增殖，并能直接抑制纯化巨噬细胞培养的HIV复制。
In vitro interactions between interleukin (IL)-12, interferon (IFN)-γ, and human immunodeficiency virus (HIV) type 1 infection in human macrophages were examined. Macrophages were infected with HIV-l and cocultured with autologous monocyte-depleted peripheral blood mononuclear cells (PBMC). The addition of autologous PBMC to HIV-1-infected macrophages resulted in an expansive increase in reverse transcriptase (RT) activity; however, when both autologous PBMC and IL-12 were added, RT activity decreased (75%–90%) and high levels of IFN-γ (9–16 ng/mL)were detected. The addition of anti-IFN-γ antibodies blocked the IL-12-induced decrease in RT activity. Surprisingly, exogenous IL-12 added to HIV-infected macrophage cultures without autologous lymphocytes resulted in a 50%–60% reduction in RT activity and no detectable increase in IFN-γ. The addition of anti-IFN-γ did not inhibit this IL-12-mediated effect. These results suggest that IL-12 is capable of indirectly down-regulating HIV proliferation in macrophage cultures reconstituted with autologous PBMC and of directly suppressing HIV replication in purified macrophage cultures.