HIV-1 and its envelope glycoprotein down-regulate chemotactic ligand receptors and chemotactic function of peripheral blood monocytes.
HIV-1 and its envelope glycoprotein down-regulate chemotactic ligand receptors and chemotactic function of peripheral blood monocytes.
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DOI：
10.4049/jimmunol.142.10.3553
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发表时间：
1989-05
影响因子：
4.4
通讯作者：
S. Wahl;J. Allen;S. Gartner;J. Orenstein;M. Popovič;D. Chenoweth;L. Arthur;W. Farrar;L. Wahl
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文献类型：
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作者：
S. Wahl;J. Allen;S. Gartner;J. Orenstein;M. Popovič;D. Chenoweth;L. Arthur;W. Farrar;L. Wahl
艾滋病患者外周血单核细胞对体外趋化刺激和体内炎症部位表现出有缺陷的迁移反应。在本研究中，正常单核细胞被体外HIV-1/HTLV-IIIBa-L分离物感染，并评估其趋化反应性。在病毒暴露后2天内，但在单核细胞产生病毒之前，趋化活性明显受损。趋化活性的降低与单核细胞表面趋化配体C5a和FMLP受体的调节有关。除HIV-1外，用纯化的HIV-1包膜糖蛋白gp120处理的单核细胞显示出对趋化配体受体和迁移功能的类似调节。此外，通过HLA-DR表达监测，诱导HIV-1或HIV-1 gp120处理的单核细胞进行分化。用特异性抗体对gp120进行免疫沉淀可逆转其对单核细胞趋化性和HLA-DR表达的影响。综上所述，这些数据表明HIV-1与单核细胞的初始相互作用不是被动的，而是HIV-1和/或HIV-1 gp120与单核细胞上的CD4R的结合转导了一个信号，导致短暂的单核细胞激活。
Peripheral blood monocytes from AIDS patients exhibit defective migratory responses to chemotactic stimuli in vitro and to inflammatory sites in vivo. In studies presented here, normal monocytes were infected with the HIV-1/HTLV-IIIBa-L isolate in vitro and evaluated for chemotactic responsiveness. Within 2 days after viral exposure, but before evidence of virus production in the monocytes, chemotactic activity was significantly impaired. Decreased chemotactic activity was associated with modulation of receptors for the chemotactic ligands, C5a and FMLP, on the monocyte cell surface. In addition to HIV-1, monocytes treated with purified HIV-1 envelope glycoprotein gp120 demonstrated a comparable modulation of chemotactic ligand receptors and migratory function. In addition, the HIV-1 or HIV-1 gp120-treated monocytes were induced to undergo differentiation as monitored by HLA-DR expression. Immunoprecipitation of the gp120 with a specific antibody reversed its effects on monocyte chemotaxis and HLA-DR expression. Taken together, these data indicate that the initial interaction of HIV-1 with the monocyte is not passive, but that the binding of HIV-1 and/or HIV-1 gp120 to the CD4R on monocytes transduces a signal leading to transient monocyte activation.