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重组HIV-1糖蛋白120对干扰素α和γ的协同诱导作用

Coordinate induction of interferon alpha and gamma by recombinant HIV-1 glycoprotein 120.

作者信息

Capobianchi M R, Ameglio F, Cordiali Fei P, Castilletti C, Mercuri F, Fais S, Dianzani F

机构信息

Institute of Virology, University La Sapienza, Rome, Italy.

出版信息

AIDS Res Hum Retroviruses. 1993 Oct;9(10):957-62. doi: 10.1089/aid.1993.9.957.

Abstract

Similarly to HIV-infected cells, recombinant HIV-1 glycoprotein 120 induces acid-labile interferon production in peripheral blood mononuclear cells from healthy donors. Acid lability of this interferon is due to the presence of both IFN-alpha and -gamma molecules. In fact, although not revealed by neutralization of antiviral activity with antibody to IFN-gamma, the presence of IFN-gamma was shown both immunoenzymatically and by detection of specific mRNA in gp120-stimulated cells. The source of IFN-gamma appears to be a T cell present in the CD4-enriched subpopulation. Cultures treated with monoclonal antibodies to the ICAM-1 and LFA-1 adhesion molecules showed an impaired release of both IFN types after gp120 stimulation, suggesting a crucial role of cell-to-cell interactions in the process leading to IFN production. Our data suggest that the HIV envelope glycoprotein could be responsible for the induction of endogenous IFN-alpha and -gamma observed in AIDS patients.

摘要

与感染HIV的细胞类似,重组HIV-1糖蛋白120可诱导健康供体外周血单核细胞产生酸不稳定的干扰素。这种干扰素的酸不稳定性归因于IFN-α和-γ分子的存在。事实上,尽管用抗IFN-γ抗体中和抗病毒活性未显示出IFN-γ的存在,但通过免疫酶法以及在gp120刺激的细胞中检测特异性mRNA均显示出IFN-γ的存在。IFN-γ的来源似乎是富含CD4的亚群中的T细胞。用抗ICAM-1和LFA-1黏附分子的单克隆抗体处理的培养物在gp120刺激后显示两种干扰素的释放受损,提示细胞间相互作用在导致干扰素产生的过程中起关键作用。我们的数据表明,HIV包膜糖蛋白可能是导致艾滋病患者体内观察到内源性IFN-α和-γ产生的原因。

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