CXCR4 and CCR5 expression on CD4+ T cells in vivo and HIV-1 antigen beta-chemokine production in vitro after treatment with HIV-1 immunogen (REMUNE).

Journal of human virology Pub Date : 2000-01-01

R B Moss, W K Giermakowska, J P Diveley, J R Savary, M R Wallace, R Z Maigetter, F C Jensen, D J Carlo

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引用次数: 0

Abstract

Background: The chemokine receptors CXCR4 and CCR5 have been identified as the major coreceptors for HIV-1 on CD4+ cells and macrophages. The natural ligands for these receptors are SDF-1 and the beta-chemokines (MIP-1alpha, MIP-1beta, RANTES), respectively, and are the products of a variety of immune cells, including CD8+ T lymphocytes.

Study design/methods: We hypothesized that the ability to stimulate the natural ligands for these receptors using an immune based therapy might influence in vivo chemokine receptor expression.

Results: In vivo CXCR4 expression remained stable after treatment with an HIV-1 Immunogen (REMUNE), whereas CCR5 expression on CD4+ T cells decreased (p < .05). Furthermore, HIV-1 antigen-specific production of beta-chemokines in vitro was also augmented (P < .05).

Conclusions: These preliminary results suggest that this HIV-1-specific immune-based therapy can stimulate antigen-specific beta-chemokine production in vitro and downregulate CCR5 receptor expression on CD4 cells in vivo.

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体内CXCR4和CCR5在CD4+ T细胞上的表达以及体外HIV-1抗原β趋化因子在HIV-1免疫原(remee)治疗后的产生。

背景:趋化因子受体CXCR4和CCR5已被确定为CD4+细胞和巨噬细胞上HIV-1的主要辅助受体。这些受体的天然配体分别是SDF-1和β趋化因子(mip -1 α、mip -1 β、RANTES)，它们是多种免疫细胞(包括CD8+ T淋巴细胞)的产物。研究设计/方法:我们假设使用免疫疗法刺激这些受体的天然配体的能力可能会影响体内趋化因子受体的表达。结果:在HIV-1免疫原治疗后，CXCR4在体内的表达保持稳定，而CCR5在CD4+ T细胞上的表达下降(p < 0.05)。此外，体外HIV-1抗原特异性趋化因子的产生也增加(P < 0.05)。结论:这些初步结果表明，这种hiv -1特异性免疫疗法可以在体外刺激抗原特异性β趋化因子的产生，并在体内下调CD4细胞上CCR5受体的表达。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Journal of human virology

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